Skip to main content

Biological roles of SLC16A1-AS1 lncRNA and its clinical impacts in tumors

Abstract

Recent studies have increasingly highlighted the aberrant expression of SLC16A1-AS1 in a variety of tumor types, where it functions as either an oncogene or a tumor suppressor in the pathogenesis of different cancers. The expression levels of SLC16A1-AS1 have been found to significantly correlate with clinical features and the prognosis of cancer patients. Furthermore, SLC16A1-AS1 modulates a range of cellular functions, including proliferation, migration, and invasion, through its interactions with diverse molecules and signaling pathways. This review examines the latest evidence regarding the role of SLC16A1-AS1 in the progression of various tumors and explores its potential clinical applications as a novel prognostic and diagnostic biomarker. Our comprehensive review aims to deepen the understanding of SLC16A1-AS1’s multifaceted role in oncology, underscoring its potential as a significant biomarker and therapeutic target.

Introduction

Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators in the complex landscape of cellular biology, gaining significant prominence in cancer research [1,2,3,4]. These RNA molecules, exceeding 200 nucleotides and lacking protein-coding capacity [5, 6], were once dismissed as “junk RNAs” [7, 8]. However, the rapid advancement of high-throughput sequencing technologies, such as RNA-Seq and single-cell sequencing techniques, along with progress in bioinformatics in recent years, have led to the identification of an increasing number of lncRNAs [9,10,11,12,13,14]. Many of these lncRNAs are now known to play vital roles in various physiological processes [15,16,17,18,19]. For example, HOTAIR, one of the earliest reported lncRNAs [20, 21], has been recognized as a significant oncogenic driver [22,23,24,25], contributing to tumor cellular signaling transduction [26,27,28], cancer metabolism reprogramming [29,30,31,32], and tumor metastasis [33,34,35,36]. Another notable lncRNA, H19, is known for its involvement in embryonic development and imprinting regulation [37,38,39,40,41,42].

LncRNAs exhibit diverse functions by participating in various cellular processes, such as cell proliferation [43,44,45], cellular metabolism [46,47,48], and cellular senescence [49, 50]. And lncRNAs often exhibit dysregulation and are implicated in a range of diseases [51,52,53,54,55], including atherosclerosis [56,57,58], Alzheimer’s disease [59,60,61], rheumatoid arthritis [62,63,64], and particularly in human tumors [65,66,67,68,69,70]. Notably, lncRNA has emerged as the promising target for the treatment of human diseases [71,72,73]. Especially with the development of CRISPR/Cas9 technology, lncRNA genes can be precisely manipulated to study their role in disease [74,75,76,77]. This helps identify new lncRNAs that are expected to become new targets and biomarkers for cancer treatment. Furthermore, the use of CRISPR/Cas9-based screens to discover lncRNAs involved in drug resistance also opens avenues for the development of more effective therapeutic strategies [78]. These advances underscore the importance of lncRNA in precision medicine and cancer treatment and mark an important step forward for customized medical solutions.

LncRNAs are broadly categorized into several types based on their genomic locations, encompassing intronic, intergenic, and antisense lncRNAs [79,80,81,82]. LncRNAs play crucial roles in regulating gene expression at multiple levels, including chromatin modification, transcription, and post-transcriptional processing [83,84,85,86,87,88]. Among these, antisense lncRNAs have recently garnered attention since their critical role in the tumor development [89, 90]. Antisense lncRNAs are types of long noncoding RNA molecules that are transcribed from the DNA strand opposite to the sense strand [91]. These RNAs can regulate gene expression through various mechanisms [89, 90, 92], including base pairing with sense RNAs, affecting their stability, translation, and splicing, or by recruiting chromatin-modifying enzymes to specific genomic regions. Their actions contribute to complex regulatory networks within cells, influencing numerous biological processes and disease states.

SLC16A1 antisense RNA 1 (SLC16A1-AS1) is a novel antisense lncRNA which has become a rising star in oncological research. SLC16A1-AS1 exhibits aberrant expression in a variety of cancers, including glioblastoma (GBM) [93, 94], oral squamous cell carcinoma (OSCC) [95, 96], hepatocellular carcinoma (HCC) [97,98,99,100], renal cell carcinoma (RCC) [101], bladder cancer [102], cervical squamous cell carcinoma(CSCC) [103], breast cancer [104,105,106], osteosarcoma [107], and non-small cell lung cancer (NSCLC) [108]. Furthermore, SLC16A1-AS1 exhibits multiple biological roles in these primary malignancies, highlighting its complexity in tumorigenesis and its potential as a tumor biomarker [93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108]. SLC16A1-AS1 is intricately linked to the proliferation, migration and invasion of tumor cells, and its abnormal expression is also related to the clinical characteristics and prognosis of cancer patients [93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108].

This article comprehensively reviews the latest findings on the role of SLC16A1-AS1 in a spectrum of human cancers, delving into its expression patterns and molecular mechanisms across different cancer types, and evaluating its viability as a prognostic and diagnostic marker. This review aims to enrich our understanding of the multifaceted role of SLC16A1-AS1 in oncology, highlighting its promise as a key biomarker and therapeutic target.

Functional roles of SLC16A1-AS1 in different tumors

SLC16A1-AS1, a tumor-associated lncRNA recently uncovered, has exhibited dysregulated expression patterns across a range of cancer types, garnering considerable interest for its potential involvement in tumor development. In vitro and in vivo investigations have illuminated the multifaceted roles of SLC16A1-AS1 in oncogenesis. These studies, utilizing an array of cell-based assays, have probed its impact on crucial cellular activities, including proliferation, apoptosis, cell cycle regulation, migration, and invasion. Table 1 summarizes the expression patterns of SLC16A1-AS1 in various tumors, highlighting their relevant functional effects and roles in cancer progression. The subsequent sections explore in detail the specific functions and regulatory mechanisms of SLC16A1-AS1 in different tumors.

Table 1 Experimental role of SLC16A1-AS1 in various cancer types

Glioblastoma

In glioblastoma, a notably aggressive form of brain tumor [109,110,111], SLC16A1-AS1 has been identified as playing a pivotal oncogenic role, as elucidated by in vitro studies. Research by Jin et al. [93] revealed that in glioblastoma cells, the lncRNA SLC16A1-AS1 regulates both mature and premature forms of miR-1269. This regulation is linked to significant changes in cancer cell behaviors, including proliferation, apoptosis, migration, and invasion, indicating SLC16A1-AS1’s role as an oncogene. Furthermore, Long et al. [94] complemented these findings by demonstrating that SLC16A1-AS1 is upregulated in glioblastoma and influences cancer cell proliferation through the epigenetic modification, specifically the methylation of miR-149. This interaction between SLC16A1-AS1 and miR-149 methylation further cements the role of SLC16A1-AS1 as an oncogene in glioblastoma. The distinct expression patterns and functional impacts of SLC16A1-AS1, involving crucial processes like microRNA regulation and methylation, not only advance our understanding of glioblastoma’s molecular mechanisms but also highlight the potential of SLC16A1-AS1 as a biomarker for glioblastoma, providing promising avenues for targeted cancer therapies and diagnostic strategies.

Oral squamous cell carcinoma

SLC16A1-AS1 plays a nuanced role in the pathogenesis of OSCC. Li et al. [95] delves into the interaction between SLC16A1-AS1 and miR-5088-5p (both mature and premature forms) in OSCC. This study indicates that SLC16A1-AS1 acts as a tumor suppressor by modulating the behavior of miR-5088-5p, which in turn affects cancer cell proliferation [95]. The specific mechanism through which SLC16A1-AS1 exerts this suppressive effect, particularly in relation to miR-5088-5p, highlights a complex interplay that could significantly influence OSCC progression.

In contrast, the findings of Feng et al. [96] portray SLC16A1-AS1 in a different light. This study does not specify an interaction with a particular miRNA but focuses on the broader tumorigenesis features of SLC16A1-AS1 in OSCC. Here, SLC16A1-AS1 is seen to contribute to cancer cell proliferation and cell cycle arrest, suggesting its role as an oncogene [96]. This oncogenic aspect of SLC16A1-AS1 in OSCC points to its potential involvement in accelerating cancer progression by disrupting normal cell cycle regulation.

These contrasting studies collectively indicate that SLC16A1-AS1 has a complex and dualistic role in OSCC. On one hand, it interacts with specific miRNAs like miR-5088-5p, potentially acting as a tumor suppressor. On the other hand, it exhibits characteristics of an oncogene, influencing cell proliferation and cell cycle processes. This duality underscores the intricate nature of SLC16A1-AS1’s involvement in OSCC and suggests that its role may vary depending on the molecular context and cellular environment. Understanding these dynamics is crucial for developing targeted therapeutic strategies for OSCC.

Hepatocellular carcinoma

SLC16A1-AS1 exhibits a complex and significant role in HCC [97,98,99]. Tian et al. [97] reported that SLC16A1-AS1 is upregulated in HCC and is associated with poor patient survival, positioning it as a potential prognostic biomarker. Furthermore, SLC16A1-AS1’s interaction with miR-141 through methylation has been shown to promote cell proliferation, characterizing it as an oncogene. This oncogenic nature is further supported by the study of Duan et al. [99], which demonstrates that SLC16A1-AS1 modulates the miR-411/MITD1 axis, affecting HCC cell viability, proliferation, migration, and invasion.

Conversely, Pei et al. [98] presented a contrasting role of SLC16A1-AS1 in HCC. Their findings suggest that SLC16A1-AS1 acts as a tumor suppressor by regulating the miR-301b-3p/CHD5 axis, impacting cell viability, proliferation, apoptosis, invasion, radiosensitivity, and the epithelial-mesenchymal transition (EMT) process. This suppression indicates a therapeutic potential for SLC16A1-AS1 in enhancing the efficacy of radiotherapy for HCC and controlling cancer progression.

These diverse findings collectively underscore the multifaceted nature of SLC16A1-AS1 in HCC. Its ability to act both as an oncogene and a tumor suppressor, depending on its interactions with specific microRNAs and the resulting cellular effects, highlights its crucial involvement in the molecular mechanisms of HCC. This dualistic nature of SLC16A1-AS1 offers insightful perspectives into potential therapeutic interventions, targeting different aspects of its function to improve treatment outcomes and patient survival in HCC.

Renal cell carcinoma

In renal cell carcinoma, SLC16A1-AS1 has been identified as playing a critical oncogenic role, as demonstrated in an in vitro study by Li et al. [101]. This study demonstrates that SLC16A1-AS1 interacts with the miR-143-3p/SLC7A11 signaling pathway, impacting crucial aspects of cancer cell behavior. These aspects include cell viability, proliferation, migration, and ferroptosis, an iron-dependent form of cell death [112, 113]. Specifically, the silencing of SLC16A1-AS1 induces ferroptosis in renal cell carcinoma cells [101]. This is mediated through an increase in miR-143-3p levels, leading to the subsequent downregulation of SLC7A11, a critical regulator of ferroptosis [114,115,116]. The normal function of SLC16A1-AS1 in renal cell carcinoma appears to be the suppression of ferroptosis, thereby promoting cell survival and proliferation. This oncogenic action of SLC16A1-AS1, through its interaction with miR-143-3p and SLC7A11, highlights its significant role in the progression and survival of renal cell carcinoma. The study underscores the potential of targeting SLC16A1-AS1 in therapeutic strategies, where manipulating its expression could promote ferroptosis in cancer cells, offering a novel approach to treat renal cell carcinoma.

Bladder cancer

In bladder cancer [102], SLC16A1-AS1 plays a significant role in cancer metabolism, closely involved in tumor progression. SLC16A1-AS1 functions both as a target and a co-activator of the transcription factor E2F1, which is known to be involved in various cellular processes [117,118,119,120,121], including cell cycle regulation and apoptosis. The interaction between SLC16A1-AS1 and E2F1 in bladder cancer leads to changes in the metabolic pathways of the cancer cells, a process termed metabolic reprogramming [122,123,124]. This reprogramming is essential for cancer cells to meet the increased energy and biosynthesis demands for rapid growth and proliferation [125,126,127]. The involvement of SLC16A1-AS1 in this process underscores its role in supporting the metabolic needs of rapidly dividing cancer cells. Furthermore, the study suggests that SLC16A1-AS1, through its interaction with E2F1, contributes to the progression of bladder cancer [102]. It may influence the expression of genes involved in metabolism, thereby facilitating the altered metabolic state that is characteristic of cancer cells. In a word, SLC16A1-AS1 in bladder cancer is implicated in several key aspects of cancer progression, particularly through its role in metabolic reprogramming, invasion, and proliferation, mediated by its interaction with E2F1 and MCT1. Understanding this intricate molecular interplay offers valuable insights into potential therapeutic targets, focusing on disrupting these crucial metabolic and proliferative pathways in bladder cancer.

Cervical squamous cell carcinoma

In CSCC, SLC16A1-AS1 functions as a key regulator in cancer cell biology, particularly influencing cell proliferation [103]. The study revealed that SLC16A1-AS1 inhibits cell proliferation in CSCC [103]. This suppression is mediated through the miR-194/SOCS2 axis, indicating a complex interaction between the lncRNA, microRNA, and downstream signaling molecules. miR-194 is known to play a role in various cellular processes and is involved in cancer progression [128,129,130]. In CSCC, SLC16A1-AS1 appears to regulate the expression or activity of miR-194, which in turn impacts the expression of SOCS2. And SOCS2 has been reported to participate in multiple cellular pathways and regulate tumor proliferation [131,132,133,134]. The downregulation of miR-194 by SLC16A1-AS1 leads to increased expression of SOCS2, which contributes to the suppression of cell proliferation.

This study sheds light on the tumor-suppressive role of SLC16A1-AS1 in CSCC, contrasting with its role in other cancer types where it may function as an oncogene. The SLC16A1-AS1/miR-194/SOCS2 axis provides a novel insight into the molecular mechanisms underlying CSCC, suggesting that modulation of this axis could be a potential therapeutic strategy in treating this type of cancer. By targeting this pathway, it may be possible to control or reduce the proliferation of CSCC cells, offering a promising avenue for future cancer therapies.

Breast cancer

In breast cancer (BC), and particularly in the context of triple-negative breast cancer (TNBC), SLC16A1-AS1 emerges as a key player, exhibiting diverse roles [104,105,106]. The research conducted by Zhao et al. [104] reported an interaction between miR-526b and SLC16A1-AS1, which significantly affects breast cancer cell proliferation, apoptosis, and invasion. This interaction suggests that miR-526b acts as an oncogene by targeting SLC16A1-AS1, highlighting a complex regulatory mechanism in TNBC. However, the study by Jiang et al. [105] demonstrates both in vitro and in vivo that the overexpression of SLC16A1-AS1 suppresses cell viability, proliferation, migration, invasion, and tumor growth in breast cancer through the miR-552-5p/WIF1 signaling pathway. This finding underscores the tumor-suppressive role of SLC16A1-AS1, which contrasts with its interaction with miR-526b and suggests a multifaceted function in different contexts of breast cancer. Additionally, Jiang et al. [106] report that SLC16A1-AS1 regulates the miR-182/PDCD4 axis, affecting cell proliferation and inducing cell cycle arrest in TNBC. This regulatory action further confirms the tumor-suppressive role of SLC16A1-AS1 in breast cancer, particularly in controlling the cell cycle and proliferation of TNBC cells. These studies collectively highlight the complex and dualistic role of SLC16A1-AS1 in breast cancer. Its interaction with different miRNAs can lead to either oncogenic or tumor-suppressive outcomes, affecting key cancer cell behaviors like proliferation, apoptosis, invasion, and tumor growth. The diverse impacts of SLC16A1-AS1 in breast cancer, particularly in TNBC, point to its potential as a multifaceted target for therapeutic interventions, with the possibility of manipulating its expression or function to impede cancer progression.

Non-small cell lung cancer

In NSCLC, in vitro studies conducted by Liu et al. [108] have identified SLC16A1-AS1 as a significant contributor to NSCLC progression. SLC16A1-AS1 plays a role in modulating the RAS/RAF/MEK signaling pathway, which is pivotal in cell growth and survival [135,136,137]. This modulation characterizes SLC16A1-AS1 as a tumor suppressor, impacting crucial cellular processes such as cell viability, proliferation, apoptosis, and cell cycle arrest in NSCLC [108]. The interaction of SLC16A1-AS1 with this signaling pathway highlights its involvement in the cellular mechanisms governing cancer progression, particularly in regulating cell growth and apoptosis. The functional significance of SLC16A1-AS1 in NSCLC underscores its importance not only in elucidating the molecular intricacies of the disease but also in its potential for targeted therapeutic strategies. Investigating the multifaceted roles of SLC16A1-AS1 could pave the way for innovative treatments and management strategies in NSCLC, potentially enhancing patient outcomes.

Prognostic and diagnostic values of SLC16A1-AS1 in different tumors

SLC16A1-AS1 has emerged as a significant biomarker with diverse clinical implications and prognostic and diagnostic values across different types of cancers (Table 2). In glioblastoma [93, 94], SLC16A1-AS1 consistently exhibits upregulation and is closely associated with key clinical features such as tumor size and stage, ultimately impacting overall survival. This upregulation pattern is consistently observed in 3 out of 4 studies on HCC [97,98,99,100]. Elevated expression of SLC16A1-AS1 in HCC samples is strongly linked to poor prognosis, including adverse outcomes in overall survival, progression-free survival, and distant metastasis-free survival [100]. Notably, Song et al. [100] demonstrated that SLC16A1-AS1 shows high sensitivity and specificity in predicting both survival and the likelihood of distant metastasis in HCC patients. Conversely, in OSCC, SLC16A1-AS1 exhibits variable expression, being both upregulated and downregulated in different studies [95, 96], with implications on histologic grades and overall survival. This variability underscores the intricate nature of SLC16A1-AS1’s role in cancer biology.

Expanding its clinical relevance, SLC16A1-AS1 displays upregulation in the stromal tissue of PDAC compared to the tumor epithelium [138]. This suggests a potential role for SLC16A1-AS1 in the remodeling of the extracellular matrix within the tumor environment. In colorectal cancer [139, 140], the upregulation of SLC16A1-AS1 in cancer tissues is significantly associated with BRAF mutation and overall survival. Additionally, it exhibits diagnostic potential in distinguishing tumor tissue from normal tissue.

In renal cell carcinoma and bladder cancer, SLC16A1-AS1 has shown diagnostic potential, particularly in bladder cancer [102], where a high AUC value suggests its effectiveness in bladder cancer diagnosis. Moreover, its upregulation is linked to poorer overall survival in renal cell carcinoma patients [101, 141].

Breast cancer presents a unique scenario where SLC16A1-AS1 exhibits a complex expression pattern, including both upregulation and downregulation in cancer tissues [104,105,106, 142]. When downregulated, it is associated with advanced clinicopathologic characteristics such as larger tumor size, higher TNM stage, and the presence of lymph node metastasis [105]. Furthermore, this downregulation correlates with unfavorable prognosis, including reduced overall survival and disease-free survival [105]. Additionally, the downregulation of SLC16A1-AS1 in the plasma of breast cancer patients suggests its potential as a circulating biomarker for diagnostic or prognostic purposes [142].

In endometrial and cervical squamous cell carcinoma, SLC16A1-AS1’s upregulation and downregulation respectively are associated with overall survival [103, 143], suggesting its role in prognostication in these cancers. Furthermore, in NSCLC [108], downregulation of SLC16A1-AS1 is linked to patient demographics, disease progression, and survival outcomes, highlighting its prognostic significance.

Recognizing the pivotal role of pathological staging in prognosis assessment, we conducted a comprehensive analysis using GEPIA2 (http://gepia2.cancer-pku.cn/#index) [144], a prominent online tool for gene expression analysis in cancer, to investigate the correlation between SLC16A1-AS1 expression levels and pathological staging across various tumors. Our initial meta-analysis of pathological staging data revealed a significant relationship between SLC16A1-AS1 expression levels and clinical stage in human tumors (Fig. 1A). Further analysis identified a significant association between SLC16A1-AS1 expression levels and pathological staging in eight specific cancer types: Bladder Urothelial Carcinoma (BLCA), Breast Invasive Carcinoma (BRCA), Head and Neck Squamous Cell Carcinoma (HNSC), Kidney Chromophobe (KICH), Kidney Renal Clear Cell Carcinoma (KIRC), Kidney Renal Papillary Cell Carcinoma (KIRP), Liver Hepatocellular Carcinoma (LIHC), and Thyroid Carcinoma (THCA) (Fig. 1B).

Fig. 1
figure 1

Association Between SLC16A1-AS1 Expression Levels and Pathological Stages of Human Tumors. (A) Meta-analysis of pathological staging data across 26 different types of tumors, providing insights into the correlation between SLC16A1-AS1 expression levels and cancer progression. (B) Significant associations in eight tumor types: Bladder Urothelial Carcinoma (BLCA), Breast Invasive Carcinoma (BRCA), Head and Neck Squamous Cell Carcinoma (HNSC), Kidney Chromophobe (KICH), Kidney Renal Clear Cell Carcinoma (KIRC), Kidney Renal Papillary Cell Carcinoma (KIRP), Liver Hepatocellular Carcinoma (LIHC), and Thyroid Carcinoma (THCA). This panel highlights specific tumor types where a significant association exists between SLC16A1-AS1 expression levels and pathological staging, offering valuable insights into the diverse roles of SLC16A1-AS1 across various cancer contexts

Overall, SLC16A1-AS1 serves as a multifaceted biomarker across various cancer types, playing a significant role in prognosis, with potential applications in diagnosis and patient stratification. The diverse expression patterns of SLC16A1-AS1 across different cancers underscore the complexity of its function in oncology and the importance of context-specific evaluations for its application in clinical practice.

Table 2 Abnormal expression of SLC16A1-AS1 and its clinical significance in different cancers

Future perspectives

SLC16A1-AS1, a complex and multifunctional lncRNA, has become a focal point in cancer research, as depicted in Fig. 2. This underscores the necessity for comprehensive research into its molecular mechanisms across a range of cancer types. SLC16A1-AS1 exerts a substantial influence on crucial cell behaviors, including cell viability, proliferation, apoptosis, cell cycle regulation, migration, invasion, tumor growth, ferroptosis, and metabolic reprogramming. Its dual functionality as either an oncogene or a tumor suppressor, depending on the cancer type and stage, highlights the importance of fully understanding its varied roles and regulatory pathways within the complex framework of cancer biology.

Fig. 2
figure 2

Regulatory Mechanisms Associated with SLC16A1-AS1 and Its Role in Different Cancers. This diagram features SLC16A1-AS1 at the center, prominently highlighted within a hexagonal frame to symbolize its central role in various cancers. Surrounding this central hexagon, rectangles represent the potential regulatory and functional interactions of SLC16A1-AS1 with various cellular processes and pathways in cancer. Each rectangle is designed to contain specific details of mechanisms of action, signaling molecules, microRNAs, or proteins that are influenced by or interact with SLC16A1-AS1. This layout underscores the complexity and multifaceted nature of SLC16A1-AS1’s impact on cellular behavior and cancer pathogenesis

However, the precise regulatory mechanisms of SLC16A1-AS1 in cancer remain elusive. Investigating its interactions with additional signaling pathways, microRNAs, and proteins is crucial for gaining a comprehensive understanding. In-depth mechanistic studies, particularly those involving in vivo research, are essential to deepen our understanding of SLC16A1-AS1’s role in tumor initiation and progression. It is also necessary to assess SLC16A1-AS1’s distinct functions and regulatory mechanisms at both the early and late stages of cancer progression. Importantly, the aberrant expression of SLC16A1-AS1, which influences malignant behaviors in tumors, suggests that targeting its expression by small molecule inhibitors, antisense oligonucleotides, or CRISPR/Cas9-based approaches could unveil new therapeutic opportunities. Moreover, SLC16A1-AS1 is implicated in the regulation of ferroptosis and metabolic reprogramming, both of which are associated with tumor drug resistance [32, 148,149,150]. Therefore, investigating the role of SLC16A1-AS1 in therapeutic resistance presents a promising avenue for future research.

It has been reported that dysregulation of SLC16A1-AS1 is associated with clinical features and prognosis in various types of tumors, as summarized in Fig. 3. Notably, the prognostic value of SLC16A1-AS1 may vary across different tumors and clinical stages. Therefore, the prognostic significance of SLC16A1-AS1 in diverse tumor types warrants further investigation through larger clinical cohorts at different cancer stages. Additionally, SLC16A1-AS1’s potential as a diagnostic marker, particularly for differentiating tumor tissue from normal tissue, is highlighted in some tumor types, such as bladder cancer [102]. However, its diagnostic efficacy in other tumor types requires more exploration. Importantly, up to now, the detection of SLC16A1-AS1 expression has been limited to tumor tissue samples. The presence of SLC16A1-AS1 in liquid biopsies, such as plasma and urine, in cancer patients remains largely unexplored. Emerging evidence suggests that some circulating lncRNAs, such as MALAT-1 [151, 152], and TUG1 [153, 154], exhibit promising diagnostic potential as non-invasive tools for cancer diagnosis. Therefore, investigating whether SLC16A1-AS1 can serve as a non-invasive tumor marker for early cancer diagnosis presents an intriguing research direction.The potential of SLC16A1-AS1 to predict disease progression, response to treatment, and patient outcomes offers substantial prospects for enhancing personalized cancer care. Integrating SLC16A1-AS1 expression profiles into clinical practice could significantly improve patient management strategies, resulting in more personalized and effective cancer treatments.

Fig. 3
figure 3

The Expression and Prognostic Network of SLC16A1-AS1 in Cancer. At the center of the diagram is SLC16A1-AS1, surrounded by a constellation of colored circles that represent its expression levels and clinical impact in various cancers. Red circles signify the upregulation of SLC16A1-AS1, while green circles indicate downregulation. The color variation of these circles not only reflects the expression levels of SLC16A1-AS1 but also underscores its prognostic significance in the oncological context

Conclusion

In conclusion, the intricate nature of SLC16A1-AS1 as a long non-coding RNA highlights its pivotal role in cancer biology, where it functions as both an oncogene and a tumor suppressor across different cancer types. This duality underscores the complexity of cancer mechanisms and reflects on SLC16A1-AS1’s significant influence on crucial cellular processes such as proliferation, apoptosis, and metastasis. The potential of SLC16A1-AS1 to serve as a novel biomarker for cancer prognosis and diagnosis represents a breakthrough in oncology, offering promising avenues for the development of targeted therapeutic interventions. Its ability to modulate key pathways in cancer cells positions it as a valuable target for innovative treatments aimed at halting cancer progression and improving patient outcomes. Moving forward, focused research on SLC16A1-AS1 will be indispensable in unraveling its multifunctional roles and in leveraging its therapeutic and diagnostic potential to combat cancer more effectively.

Data availability

No datasets were generated or analysed during the current study.

References

  1. Huarte M. The emerging role of lncRNAs in cancer. Nat Med. 2015;21(11):1253–61.

    Article  CAS  PubMed  Google Scholar 

  2. Zhao S, et al. Long noncoding RNAs: fine-tuners hidden in the cancer signaling network. Cell Death Discov. 2021;7(1):283.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Xu Y, et al. The emerging regulatory roles of long non-coding RNAs implicated in cancer metabolism. Mol Ther. 2021;29(7):2209–18.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Zhang ZD, et al. Long non–coding RNAs, lipid metabolism and cancer (review). Exp Ther Med. 2023;26(4):470.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Jarroux J, Morillon A, Pinskaya M. History, Discovery, and classification of lncRNAs. Adv Exp Med Biol. 2017;1008:1–46.

    Article  CAS  PubMed  Google Scholar 

  6. Perkel JM, Visiting noncodarnia. Biotechniques. 2013;54(6):301.

    Article  CAS  PubMed  Google Scholar 

  7. Louro R, Smirnova AS, Verjovski-Almeida S. Long intronic noncoding RNA transcription: expression noise or expression choice? Genomics. 2009;93(4):291–8.

    Article  CAS  PubMed  Google Scholar 

  8. Mattick JS, Makunin IV. Non-coding RNA. Hum Mol Genet, 2006. 15 Spec No 1: p. R17-29.

  9. Gao N, et al. Long non-coding RNAs: the Regulatory mechanisms, Research Strategies, and future directions in cancers. Front Oncol. 2020;10:598817.

    Article  PubMed  PubMed Central  Google Scholar 

  10. Gong Y, et al. Bioinformatics Analysis of Long non-coding RNA and related diseases: an overview. Front Genet. 2021;12:813873.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Agnelli L, Bortoluzzi S, Pruneri G. Bioinformatic pipelines to analyze lncRNAs RNAseq Data. Methods Mol Biol. 2021;2348:55–69.

    Article  CAS  PubMed  Google Scholar 

  12. Chu C, Spitale RC, Chang HY. Technologies to probe functions and mechanisms of long noncoding RNAs. Nat Struct Mol Biol. 2015;22(1):29–35.

    Article  CAS  PubMed  Google Scholar 

  13. Signal B, Gloss BS, Dinger ME. Computational approaches for functional prediction and characterisation of long noncoding RNAs. Trends Genet. 2016;32(10):620–37.

    Article  CAS  PubMed  Google Scholar 

  14. Iwakiri J, Hamada M, Asai K. Bioinformatics tools for lncRNA research. Biochim Biophys Acta. 2016;1859(1):23–30.

    Article  CAS  PubMed  Google Scholar 

  15. Wu Y, Xu X. Long non-coding RNA signature in colorectal cancer: research progression and clinical application. Cancer Cell Int. 2023;23(1):28.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Pan X, Li C, Feng J. The role of LncRNAs in tumor immunotherapy. Cancer Cell Int. 2023;23(1):30.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Hu SP, et al. LncRNA HCP5 as a potential therapeutic target and prognostic biomarker for various cancers: a meta–analysis and bioinformatics analysis. Cancer Cell Int. 2021;21(1):686.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Zhang L, Sun H, Chen X. Long noncoding RNAs in human reproductive processes and diseases. Mol Reprod Dev. 2024;91(1):e23728.

    Article  CAS  PubMed  Google Scholar 

  19. Tavares ESJ et al. The impact of long noncoding RNAs in tissue regeneration and senescence. Cells, 2024. 13(2).

  20. Woo CJ, Kingston RE. HOTAIR lifts noncoding RNAs to new levels. Cell. 2007;129(7):1257–9.

    Article  CAS  PubMed  Google Scholar 

  21. Rinn JL, et al. Functional demarcation of active and silent chromatin domains in human HOX loci by noncoding RNAs. Cell. 2007;129(7):1311–23.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Rajagopal T, et al. HOTAIR LncRNA: a novel oncogenic propellant in human cancer. Clin Chim Acta. 2020;503:1–18.

    Article  CAS  PubMed  Google Scholar 

  23. Hajjari M, Salavaty A. HOTAIR: an oncogenic long non-coding RNA in different cancers. Cancer Biol Med. 2015;12(1):1–9.

    CAS  PubMed  PubMed Central  Google Scholar 

  24. Kuo FC, et al. LncRNA HOTAIR impairs the prognosis of papillary thyroid cancer via regulating cellular malignancy and epigenetically suppressing DLX1. Cancer Cell Int. 2022;22(1):396.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Li J, et al. HOTAIR: a key regulator in gynecologic cancers. Cancer Cell Int. 2017;17:65.

    Article  PubMed  PubMed Central  Google Scholar 

  26. Hakami MA, et al. A key regulator of the Wnt/β-catenin signaling cascade in cancer progression and treatment. Pathol Res Pract. 2024;253:154957.

    Article  CAS  PubMed  Google Scholar 

  27. Wang J, et al. Long noncoding RNA HOTAIR regulates the stemness of breast cancer cells via activation of the NF-κB signaling pathway. J Biol Chem. 2022;298(12):102630.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Sadeghalvad M, et al. Long non-coding RNA HOTAIR induces the PI3K/AKT/mTOR signaling pathway in breast cancer cells. Rev Assoc Med Bras (1992). 2022;68(4):456–62.

    Article  PubMed  Google Scholar 

  29. Ma Y, et al. Long non-coding RNA HOTAIR promotes cancer cell energy metabolism in pancreatic adenocarcinoma by upregulating hexokinase-2. Oncol Lett. 2019;18(3):2212–9.

    CAS  PubMed  PubMed Central  Google Scholar 

  30. Hu M, et al. LncRNA HOTAIR knockdown inhibits glycolysis by regulating miR-130a-3p/HIF1A in hepatocellular carcinoma under hypoxia. Biomed Pharmacother. 2020;125:109703.

    Article  CAS  PubMed  Google Scholar 

  31. Wei S, et al. Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling. Oncol Rep. 2017;38(3):1902–8.

    Article  CAS  PubMed  Google Scholar 

  32. Wang K, et al. Role of long non-coding RNAs in metabolic reprogramming of gastrointestinal cancer cells. Cancer Cell Int. 2024;24(1):15.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Ma Q et al. Inducible lncRNA transgenic mice reveal continual role of HOTAIR in promoting breast cancer metastasis. Elife, 2022. 11.

  34. Wan Y, Chang HY. Flight of noncoding RNAs in cancer metastasis. Cell Cycle. 2010;9(17):3391–2.

    Article  CAS  PubMed  Google Scholar 

  35. Gupta RA, et al. Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Nature. 2010;464(7291):1071–6.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Chen L, et al. The HOTAIR lncRNA: a remarkable oncogenic promoter in human cancer metastasis. Oncol Lett. 2021;21(4):302.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Zhu JQ, et al. Sodium fluoride disrupts DNA methylation of H19 and Peg3 imprinted genes during the early development of mouse embryo. Arch Toxicol. 2014;88(2):241–8.

    Article  CAS  PubMed  Google Scholar 

  38. Ratajczak MZ. Igf2-H19, an imprinted tandem gene, is an important regulator of embryonic development, a guardian of proliferation of adult pluripotent stem cells, a regulator of longevity, and a ‘passkey’ to cancerogenesis. Folia Histochem Cytobiol. 2012;50(2):171–9.

    Article  CAS  PubMed  Google Scholar 

  39. Tabano S, et al. Epigenetic modulation of the IGF2/H19 imprinted domain in human embryonic and extra-embryonic compartments and its possible role in fetal growth restriction. Epigenetics. 2010;5(4):313–24.

    Article  CAS  PubMed  Google Scholar 

  40. Gabory A, Jammes H, Dandolo L. The H19 locus: role of an imprinted non-coding RNA in growth and development. BioEssays. 2010;32(6):473–80.

    Article  CAS  PubMed  Google Scholar 

  41. Gabory A, et al. The H19 gene: regulation and function of a non-coding RNA. Cytogenet Genome Res. 2006;113(1–4):188–93.

    Article  CAS  PubMed  Google Scholar 

  42. Viville S, Surani MA. Towards unravelling the Igf2/H19 imprinted domain. BioEssays. 1995;17(10):835–8.

    Article  CAS  PubMed  Google Scholar 

  43. Feng J, et al. Inhibition of lncRNA PCAT19 promotes breast cancer proliferation. Cancer Med. 2023;12(10):11971–82.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Yu L, et al. lncRNA-HIT promotes cell proliferation of non-small cell lung cancer by association with E2F1. Cancer Gene Ther. 2017;24(5):221–6.

    Article  CAS  PubMed  Google Scholar 

  45. Zhang J, et al. Lnc-LRRTM4 promotes proliferation, metastasis and EMT of colorectal cancer through activating LRRTM4 transcription. Cancer Cell Int. 2023;23(1):142.

    Article  PubMed  PubMed Central  Google Scholar 

  46. Lin W, et al. LncRNAs regulate metabolism in cancer. Int J Biol Sci. 2020;16(7):1194–206.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Tao T et al. The molecular mechanisms of LncRNA-correlated PKM2 in cancer metabolism. Biosci Rep, 2019. 39(11).

  48. Guo Y, et al. Role of LncRNAs in regulating cancer amino acid metabolism. Cancer Cell Int. 2021;21(1):209.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. Chen D, et al. LncRNA NEAT1 suppresses cellular senescence in hepatocellular carcinoma via KIF11-dependent repression of CDKN2A. Clin Transl Med. 2023;13(9):e1418.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  50. Degirmenci U, Lei S. Role of lncRNAs in Cellular Aging. Front Endocrinol (Lausanne). 2016;7:151.

    Article  PubMed  Google Scholar 

  51. Wang PS, Wang Z, Yang C. Dysregulations of long non-coding RNAs - the emerging lnc in environmental carcinogenesis. Semin Cancer Biol. 2021;76:163–72.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Nemeth K et al. Non-coding RNAs in disease: from mechanisms to therapeutics. Nat Rev Genet, 2023.

  53. Ghasemian M, Poodineh J. A review on the biological roles of LncRNA PTCSC3 in cancerous and non-cancerous disorders. Cancer Cell Int. 2023;23(1):184.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Li C, et al. Roles and mechanisms of exosomal non-coding RNAs in human health and diseases. Signal Transduct Target Ther. 2021;6(1):383.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Ghasemian M, et al. Long non-coding RNA MIR4435-2HG: a key molecule in progression of cancer and non-cancerous disorders. Cancer Cell Int. 2022;22(1):215.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  56. Ma Y, et al. LncRNA: an important Regulator of Atherosclerosis. Curr Med Chem. 2023;30(38):4340–54.

    Article  CAS  PubMed  Google Scholar 

  57. Mao Y, Yue H, Dong F. LncRNA CDKN2B-AS1 in atherosclerosis: friend or foe? Int J Cardiol. 2021;343:106.

    Article  PubMed  Google Scholar 

  58. Bian W, et al. Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis. Aging. 2020;12(7):6385–400.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  59. Li Y, et al. Targeting lncRNA NEAT1 hampers Alzheimer’s Disease Progression. Neuroscience. 2023;529:88–98.

    Article  CAS  PubMed  Google Scholar 

  60. Balusu S, et al. MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer’s disease. Science. 2023;381(6663):1176–82.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  61. Maoz R, Garfinkel BP, Soreq H. Alzheimer’s Disease and ncRNAs. Adv Exp Med Biol. 2017;978:337–61.

    Article  CAS  PubMed  Google Scholar 

  62. Lei HT, et al. LncRNA-mediated cell autophagy: an emerging field in bone destruction in rheumatoid arthritis. Biomed Pharmacother. 2023;168:115716.

    Article  CAS  PubMed  Google Scholar 

  63. Yang J, et al. The role of non-coding RNAs (miRNA and lncRNA) in the clinical management of rheumatoid arthritis. Pharmacol Res. 2022;186:106549.

    Article  CAS  PubMed  Google Scholar 

  64. Li Z et al. Long non-coding RNAs in rheumatoid arthritis. Cell Prolif, 2018. 51(1).

  65. Zeng H, et al. LncRNA SNHG1: role in tumorigenesis of multiple human cancers. Cancer Cell Int. 2023;23(1):198.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  66. Lv N, et al. Long noncoding RNAs: glycolysis regulators in gynaecologic cancers. Cancer Cell Int. 2023;23(1):4.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Liu F, et al. Long non-coding RNA ZFAS1 correlates with clinical progression and prognosis in cancer patients. Oncotarget. 2017;8(37):61561–9.

    Article  PubMed  PubMed Central  Google Scholar 

  68. Ouyang J, et al. Long non-coding RNAs are involved in alternative splicing and promote cancer progression. Br J Cancer. 2022;126(8):1113–24.

    Article  CAS  PubMed  Google Scholar 

  69. Najafi S, et al. Long non-coding RNAs (lncRNAs); roles in tumorigenesis and potentials as biomarkers in cancer diagnosis. Exp Cell Res. 2022;418(2):113294.

    Article  CAS  PubMed  Google Scholar 

  70. Liu FT, et al. Prognostic value of long non-coding RNA UCA1 in human solid tumors. Oncotarget. 2016;7(36):57991–8000.

    Article  PubMed  PubMed Central  Google Scholar 

  71. Chen Y, et al. Long non-coding RNAs: from disease code to drug role. Acta Pharm Sin B. 2021;11(2):340–54.

    Article  CAS  PubMed  Google Scholar 

  72. Pierce JB, et al. Long noncoding RNAs as therapeutic targets. Adv Exp Med Biol. 2022;1363:161–75.

    Article  CAS  PubMed  Google Scholar 

  73. Nemeth K, et al. Non-coding RNAs in disease: from mechanisms to therapeutics. Nat Rev Genet. 2024;25(3):211–32.

    Article  CAS  PubMed  Google Scholar 

  74. Xing H, Meng L-h. CRISPR-cas9: a powerful tool towards precision medicine in cancer treatment. Acta Pharmacol Sin. 2020;41(5):583–7.

    Article  CAS  PubMed  Google Scholar 

  75. Srinivas T, Siqueira E, Guil S. Techniques for investigating lncRNA transcript functions in neurodevelopment. Mol Psychiatry, 2023.

  76. Mahato RK, et al. Targeting long non-coding RNAs in cancer therapy using CRISPR-Cas9 technology: a novel paradigm for precision oncology. J Biotechnol. 2024;379:98–119.

    Article  CAS  PubMed  Google Scholar 

  77. M SZ, Hartford CCR, Lal A. Interrogating lncRNA functions via CRISPR/Cas systems. RNA Biol. 2021;18(12):2097–106.

    Article  Google Scholar 

  78. Chan YT, et al. CRISPR-Cas9 library screening approach for anti-cancer drug discovery: overview and perspectives. Theranostics. 2022;12(7):3329–44.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  79. Mattick JS, et al. Long non-coding RNAs: definitions, functions, challenges and recommendations. Nat Rev Mol Cell Biol. 2023;24(6):430–47.

    Article  CAS  PubMed  Google Scholar 

  80. Policarpo R, et al. From junk to function: LncRNAs in CNS health and disease. Front Mol Neurosci. 2021;14:714768.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  81. Ma L, Bajic VB, Zhang Z. On the classification of long non-coding RNAs. RNA Biol. 2013;10(6):925–33.

    Article  PubMed  Google Scholar 

  82. Yousefi H, et al. Long noncoding RNAs and exosomal lncRNAs: classification, and mechanisms in breast cancer metastasis and drug resistance. Oncogene. 2020;39(5):953–74.

    Article  CAS  PubMed  Google Scholar 

  83. Sebastian-delaCruz M et al. The role of lncRNAs in Gene expression regulation through mRNA stabilization. Noncoding RNA, 2021. 7(1).

  84. Statello L, et al. Gene regulation by long non-coding RNAs and its biological functions. Nat Rev Mol Cell Biol. 2021;22(2):96–118.

    Article  CAS  PubMed  Google Scholar 

  85. Bhat SA, et al. Long non-coding RNAs: mechanism of action and functional utility. Noncoding RNA Res. 2016;1(1):43–50.

    Article  PubMed  PubMed Central  Google Scholar 

  86. Han P, Chang CP. Long non-coding RNA and chromatin remodeling. RNA Biol. 2015;12(10):1094–8.

    Article  PubMed  PubMed Central  Google Scholar 

  87. Pisignano G, Ladomery M. Post-transcriptional regulation through long non-coding RNAs (lncRNAs). Noncoding RNA, 2021. 7(2).

  88. Long Y, et al. How do lncRNAs regulate transcription? Sci Adv. 2017;3(9):eaao2110.

    Article  PubMed  PubMed Central  Google Scholar 

  89. Liu B, et al. The regulatory role of antisense lncRNAs in cancer. Cancer Cell Int. 2021;21(1):459.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  90. Zhou M, et al. The patterns of antisense long non-coding RNAs regulating corresponding sense genes in human cancers. J Cancer. 2021;12(5):1499–506.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  91. Bhan A, Soleimani M, Mandal SS. Long noncoding RNA and Cancer: a New Paradigm. Cancer Res. 2017;77(15):3965–81.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  92. Rehman SU, et al. Recent insights into the functions and mechanisms of antisense RNA: emerging applications in cancer therapy and precision medicine. Front Chem. 2023;11:1335330.

    Article  PubMed  Google Scholar 

  93. Jin Z, et al. MicroRNA-1269 is downregulated in glioblastoma and its maturation is regulated by long non-coding RNA SLC16A1 antisense RNA 1. Bioengineered. 2022;13(5):12749–59.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  94. Long Y, et al. LncRNA SLC16A1-AS1 is upregulated in Glioblastoma and promotes Cancer Cell Proliferation by regulating miR-149 methylation. Cancer Manag Res. 2021;13:1215–23.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  95. Li T, Wang D, Yang S. Analysis of the subcellular location of lncRNA SLC16A1-AS1 and its interaction with premature mir-5088-5p in oral squamous cell carcinoma. Odontology. 2023;111(1):41–8.

    Article  CAS  PubMed  Google Scholar 

  96. Feng H, et al. Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma. Cell Cycle. 2020;19(13):1641–53.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  97. Tian J, Hu D. LncRNA SLC16A1-AS1 is upregulated in hepatocellular carcinoma and predicts poor survival. Clin Res Hepatol Gastroenterol. 2021;45(2):101490.

    Article  CAS  PubMed  Google Scholar 

  98. Pei S, et al. SLC16A1-AS1 enhances radiosensitivity and represses cell proliferation and invasion by regulating the miR-301b-3p/CHD5 axis in hepatocellular carcinoma. Environ Sci Pollut Res Int. 2020;27(34):42778–90.

    Article  CAS  PubMed  Google Scholar 

  99. Duan C. LncRNA SLC16A1-AS1 contributes to the progression of hepatocellular carcinoma cells by modulating miR-411/MITD1 axis. J Clin Lab Anal. 2022;36(4):e24344.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  100. Song M, et al. Large-scale analyses identify a cluster of novel long noncoding RNAs as potential competitive endogenous RNAs in progression of hepatocellular carcinoma. Aging. 2019;11(22):10422–53.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  101. Li YZ, et al. Silencing lncRNA SLC16A1-AS1 Induced Ferroptosis in Renal Cell Carcinoma through miR-143-3p/SLC7A11 signaling. Technol Cancer Res Treat. 2022;21:15330338221077803.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  102. Logotheti S, et al. LncRNA-SLC16A1-AS1 induces metabolic reprogramming during bladder Cancer progression as target and co-activator of E2F1. Theranostics. 2020;10(21):9620–43.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  103. Zhang H, et al. LncRNA SLC16A1-AS1 suppresses cell proliferation in cervical squamous cell carcinoma (CSCC) through the miR-194/SOCS2 Axis. Cancer Manag Res. 2021;13:1299–306.

    Article  PubMed  PubMed Central  Google Scholar 

  104. Zhao X, et al. MiR-526b targets lncRNA SLC16A1-AS1 to suppress cell proliferation in triple-negative breast cancer. J Biochem Mol Toxicol. 2023;37(3):e23247.

    Article  CAS  PubMed  Google Scholar 

  105. Jiang B, Xia J, Zhou X. Overexpression of lncRNA SLC16A1-AS1 suppresses the growth and metastasis of breast Cancer via the miR-552-5p/WIF1 signaling pathway. Front Oncol. 2022;12:712475.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  106. Jiang B, et al. LncRNA SLC16A1-AS1 regulates the miR-182/PDCD4 axis and inhibits the triple-negative breast cancer cell cycle. Immunopharmacol Immunotoxicol. 2022;44(4):534–40.

    Article  CAS  PubMed  Google Scholar 

  107. Rothzerg E et al. Upregulation of 15 antisense long non-coding RNAs in Osteosarcoma. Genes (Basel), 2021. 12(8).

  108. Liu HY, et al. lncRNA SLC16A1-AS1 as a novel prognostic biomarker in non-small cell lung cancer. J Investig Med. 2020;68(1):52–9.

    Article  PubMed  Google Scholar 

  109. Wang G, Wang W. Advanced Cell therapies for Glioblastoma. Front Immunol. 2022;13:904133.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  110. Davis ME. Glioblastoma: overview of Disease and Treatment. Clin J Oncol Nurs. 2016;20(5 Suppl):S2–8.

    Article  PubMed  PubMed Central  Google Scholar 

  111. Domingo-Musibay E, Galanis E. What next for newly diagnosed glioblastoma? Future Oncol. 2015;11(24):3273–83.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  112. Dixon SJ, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell. 2012;149(5):1060–72.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  113. Hirschhorn T, Stockwell BR. The development of the concept of ferroptosis. Free Radic Biol Med. 2019;133:130–43.

    Article  CAS  PubMed  Google Scholar 

  114. Lee J, Roh JL. SLC7A11 as a gateway of metabolic perturbation and ferroptosis vulnerability in Cancer. Antioxid (Basel), 2022. 11(12).

  115. Koppula P, Zhuang L, Gan B. Cystine transporter SLC7A11/xCT in cancer: ferroptosis, nutrient dependency, and cancer therapy. Protein Cell. 2021;12(8):599–620.

    Article  CAS  PubMed  Google Scholar 

  116. Lin W, et al. SLC7A11/xCT in cancer: biological functions and therapeutic implications. Am J Cancer Res. 2020;10(10):3106–26.

    CAS  PubMed  PubMed Central  Google Scholar 

  117. Denechaud PD, Fajas L, Giralt A. E2F1, a Novel Regulator of Metabolism. Front Endocrinol (Lausanne). 2017;8:311.

    Article  PubMed  Google Scholar 

  118. Gao S, et al. The mir-532-E2F1 feedback loop contributes to gastric cancer progression. Cell Death Dis. 2022;13(4):376.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  119. Zu ML, et al. Gypenoside LI arrests the cell cycle of breast cancer in G0/G1 phase by down-regulating E2F1. J Ethnopharmacol. 2021;273:114017.

    Article  CAS  PubMed  Google Scholar 

  120. Li P, et al. E2F transcription factor 1 is involved in the phenotypic modulation of esophageal squamous cell carcinoma cells via microRNA-375. Bioengineered. 2021;12(2):10047–62.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  121. Shen C, et al. [Advancement of E2F1 in Common Tumors]. Zhongguo Fei Ai Za Zhi. 2020;23(10):921–6.

    PubMed  Google Scholar 

  122. Ohshima K, Morii E. Metabolic reprogramming of Cancer cells during Tumor Progression and Metastasis. Metabolites, 2021. 11(1).

  123. Martínez-Reyes I, Chandel NS. Cancer metabolism: looking forward. Nat Rev Cancer. 2021;21(10):669–80.

    Article  PubMed  Google Scholar 

  124. Faubert B, Solmonson A, DeBerardinis RJ. Metabolic reprogramming and cancer progression. Science, 2020. 368(6487).

  125. Zhu J, Thompson CB. Metabolic regulation of cell growth and proliferation. Nat Rev Mol Cell Biol. 2019;20(7):436–50.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  126. Schiliro C, Firestein BL. Mechanisms of metabolic reprogramming in Cancer cells supporting enhanced growth and proliferation. Cells, 2021. 10(5).

  127. DeBerardinis RJ, et al. The Biology of Cancer: metabolic reprogramming fuels cell growth and proliferation. Cell Metabol. 2008;7(1):11–20.

    Article  CAS  Google Scholar 

  128. Wang B, et al. MiR-194, commonly repressed in colorectal cancer, suppresses tumor growth by regulating the MAP4K4/c-Jun/MDM2 signaling pathway. Cell Cycle. 2015;14(7):1046–58.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  129. Huang P, et al. Genome-wide association studies identify miRNA-194 as a prognostic biomarker for gastrointestinal cancer by targeting ATP6V1F, PPP1R14B, BTF3L4 and SLC7A5. Front Oncol. 2022;12:1025594.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  130. Yin W, Shi L, Mao Y. MiR-194 regulates nasopharyngeal carcinoma progression by modulating MAP3K3 expression. FEBS Open Bio. 2019;9(1):43–52.

    Article  CAS  PubMed  Google Scholar 

  131. Vitali C, et al. SOCS2 controls proliferation and stemness of Hematopoietic Cells under stress conditions and its Deregulation Marks unfavorable Acute Leukemias. Cancer Res. 2015;75(11):2387–99.

    Article  CAS  PubMed  Google Scholar 

  132. Jian F, et al. The long-noncoding RNA SOCS2-AS1 suppresses endometrial cancer progression by regulating AURKA degradation. Cell Death Dis. 2021;12(4):351.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  133. Cabrera-Galván JJ, et al. SOCS2 protects against chemical-induced hepatocellular carcinoma progression by modulating inflammation and cell proliferation in the liver. Biomed Pharmacother. 2023;157:114060.

    Article  PubMed  Google Scholar 

  134. Masuzaki R et al. Suppressors of Cytokine Signaling and Hepatocellular Carcinoma. Cancers (Basel), 2022. 14(10).

  135. Wan W, et al. Isoprenylcysteine carboxyl methyltransferase is critical for glioblastoma growth and survival by activating Ras/Raf/Mek/Erk. Cancer Chemother Pharmacol. 2022;89(3):401–11.

    Article  CAS  PubMed  Google Scholar 

  136. Steelman LS, et al. Roles of the Ras/Raf/MEK/ERK pathway in leukemia therapy. Leukemia. 2011;25(7):1080–94.

    Article  CAS  PubMed  Google Scholar 

  137. McCubrey JA, et al. Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy. Leukemia. 2008;22(4):708–22.

    Article  CAS  PubMed  Google Scholar 

  138. Ufuk A et al. Monocarboxylate transporters are involved in Extracellular Matrix Remodelling in Pancreatic Ductal Adenocarcinoma. Cancers (Basel), 2022. 14(5).

  139. Poursheikhani A, Abbaszadegan MR, Kerachian MA. Long non-coding RNA AC087388.1 as a novel biomarker in colorectal cancer. BMC Cancer. 2022;22(1):196.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  140. Poursheikhani A, et al. Integration analysis of long non-coding RNA (lncRNA) role in tumorigenesis of colon adenocarcinoma. BMC Med Genomics. 2020;13(1):108.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  141. Gong M, et al. Upregulation of BMP1 through ncRNAs correlates with adverse outcomes and immune infiltration in clear cell renal cell carcinoma. Eur J Med Res. 2023;28(1):440.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  142. Wang H, et al. Novel lncRNAs with diagnostic or prognostic value screened out from breast cancer via bioinformatics analyses. PeerJ. 2022;10:e13641.

    Article  PubMed  PubMed Central  Google Scholar 

  143. Zhou X, et al. m6A-related long noncoding RNAs predict prognosis and indicate therapeutic response in endometrial carcinoma. J Clin Lab Anal. 2023;37(1):e24813.

    Article  CAS  PubMed  Google Scholar 

  144. Tang Z, et al. GEPIA2: an enhanced web server for large-scale expression profiling and interactive analysis. Nucleic Acids Res. 2019;47(W1):W556–w560.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  145. Liu S, et al. COLGALT1 is a potential biomarker for predicting prognosis and immune responses for kidney renal clear cell carcinoma and its mechanisms of ceRNA networks. Eur J Med Res. 2022;27(1):122.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  146. Bohosova J, et al. LncRNA PVT1 is increased in renal cell carcinoma and affects viability and migration in vitro. J Clin Lab Anal. 2022;36(6):e24442.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  147. Xiong Y, et al. The VIM-AS1/miR-655/ZEB1 axis modulates bladder cancer cell metastasis by regulating epithelial-mesenchymal transition. Cancer Cell Int. 2021;21(1):233.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  148. Zhang C, et al. Ferroptosis in cancer therapy: a novel approach to reversing drug resistance. Mol Cancer. 2022;21(1):47.

    Article  PubMed  PubMed Central  Google Scholar 

  149. Friedmann Angeli JP, Krysko DV, Conrad M. Ferroptosis at the crossroads of cancer-acquired drug resistance and immune evasion. Nat Rev Cancer. 2019;19(7):405–14.

    Article  CAS  PubMed  Google Scholar 

  150. Roh J et al. The involvement of long non-coding RNAs in glutamine-metabolic reprogramming and therapeutic resistance in Cancer. Int J Mol Sci, 2022. 23(23).

  151. Weber DG, et al. Evaluation of long noncoding RNA MALAT1 as a candidate blood-based biomarker for the diagnosis of non-small cell lung cancer. BMC Res Notes. 2013;6:518.

    Article  PubMed  PubMed Central  Google Scholar 

  152. Ren S, et al. Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 derived miniRNA as a novel plasma-based biomarker for diagnosing prostate cancer. Eur J Cancer. 2013;49(13):2949–59.

    Article  CAS  PubMed  Google Scholar 

  153. Mohyeldeen M, et al. Serum expression and diagnostic potential of long non-coding RNAs NEAT1 and TUG1 in viral hepatitis C and viral hepatitis C-associated hepatocellular carcinoma. Clin Biochem. 2020;84:38–44.

    Article  CAS  PubMed  Google Scholar 

  154. Yin Q, et al. Elevated serum lncRNA TUG1 levels are a potential diagnostic biomarker of multiple myeloma. Exp Hematol. 2019;79:47–55e2.

    Article  CAS  PubMed  Google Scholar 

Download references

Funding

This study was supported by grants to Xi Ouyang from by the National Natural Science Foundation of China (No.82060279), and Bing Liao by the Natural Science Foundation of Jiangxi Province (20232BAB206118).

Author information

Authors and Affiliations

Authors

Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Corresponding author

Correspondence to Xi Ouyang.

Ethics declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Liao, B., Wang, J., Yuan, Y. et al. Biological roles of SLC16A1-AS1 lncRNA and its clinical impacts in tumors. Cancer Cell Int 24, 122 (2024). https://doi.org/10.1186/s12935-024-03285-6

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12935-024-03285-6

Keywords