Skip to main content
Download PDF

A review on the role of LINC01133 in cancers

Cancer Cell International volume 22, Article number: 270 (2022) Cite this article

Abstract

Long Intergenic Non-Protein Coding RNA 1133 (LINC01133) is a long non-coding RNA (lncRNA) which interacts with miR-106a-3p, miR-576-5p, miR-495-3p, miR-205, miR-199a-5p, miR-4784, miR-30a-5p, miR-199a, miR-30b-5p, miR-216a -5p and miR-422a, thus increasing expression of mRNA targets of these miRNAs. LINC01133 can affect cancer metastasis through regulation of epithelial-mesenchymal transition program. Dysregulation of this lncRNA has been repeatedly detected in the process of tumorigenesis. In this review, we summarize the results of various studies that reported dysregulation of LINC01133 in different samples and described the role of this lncRNA as a marker for these disorders.

Introduction

Long non-coding RNAs (lncRNAs) have been vastly investigated for their effects in the carcinogenesis [1]. These transcripts have sizes larger than 200 nt and are mainly located in the nucleus [2]. Although lncRNAs are expressed at low levels, they participate in transcriptional and post-transcriptional regulation of gene expression via interacting with other types of biomolecules, namely nucleic acids or proteins [3]. They can enhance or interfere with establishment of transcription loops. Moreover, they are able to induce or suppress recruitment of other regulators [4, 5] and affect mRNA splicing. Finally, they serve as origin for microRNAs (miRNAs) [6]. Notably, lncRNAs can affect tumorigenesis through acting as oncogenes or tumor suppressors [7].

Long Intergenic Non-Protein Coding RNAs (LINC RNAs), as a class of lncRNAs have been found to interplay with chromatin modification complexes or RNA binding proteins [8]. These transcripts can change gene expression programs. Previous studies have reported distinctive expression profile of LINC RNAs in primary and metastatic tumors [8, 9] and the role of these transcripts in the metastases [10,11,12]. Moreover, expression of these transcripts is finely controlled in the course of development and in response to different signals [13]. LINC01133 is an example of these transcripts. The gene coding this lncRNA is located on 1q23.2. This lncRNA has four transcript variants with sizes of 1996 bp, 1418 bp, 1405 bp and 1266 bp, respectively (http://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000224259;r=1:159958035-159984750).

LINC01133 has been found to be dysregulated in the process of tumorigenesis. However, it has different patterns of expression in various malignancies, or even within a certain type of malignancy. In this review, we summarize the results of various studies that reported dysregulation of LINC01133 in cell line originated from different cancer types, animal studies and investigations in human samples.

Cell line studies

In vitro and functional studies in different cell lines have reported either oncogenic (Fig. 1) or tumor suppressor role (Fig. 2) for LINC01133. In the following sections, we describe the role of LINC01133 in different cancers.

Gynecological cancers

Expression of LINC01133 has been found to be enhanced in epithelial ovarian cancer cell lines. Functionally, LINC01133 enhances migration and invasiveness of ovarian cancer cells. LINC01133 and miR-495-3p have been shown to reciprocally repress expression of each other. LINC01133 can interact with miR-495-3p to enhance metastatic ability of ovarian cancer cells via regulation of TPD52 [14]. A microarray-based study in ovarian cancer has shown differential expression of LINC01133 and miR-205 in ovarian cancer samples versus non-cancerous samples [15]. Contrary to the study conducted by Liu et al. [14], LINC01133 has been shown to repress proliferation, invasiveness and migration of ovarian cancer cells [15]. Functionally, LINC01133 could bind with miR-205 and subsequently regulate expression of LRRK2 [15].

Over-expression of LINC01133 in cervical cancer cells has increased their proliferation and metastatic ability while reducing their apoptosis. LINC01133 silencing has inhibited their malignant phenotype. Functionally, up-regulation of LINC01133 results in reduction of miR-30a-5p levels and enhancement of FOXD1 levels [16].

LINC01133 has also been shown to regulate malignant behavior of triple negative breast cancer cells. In fact, LINC01133 could sufficiently promote phenotypic and growth features of cancer stem cells. This lncRNA directly mediates the mesenchymal stem/stromal cells-induced miR-199a-FOXP2 axis. LINC01133 can also regulate expression of the pluripotency-determining gene KLF4 [17].

LINC01133 has also been revealed to be up-regulated in pancreatic cancer cells in association with higher DKK1 methylation and up-regulation of genes involved in the Wnt signaling pathway. LINC01133 binds with DKK1 promoter, inducing H3K27 trimethylation and decreasing its expression. However, Wnt-5a, MMP-7, and β-catenin levels have been found to be up-regulated following LINC01133 binding. Over-expression of LINC01133 has promoted proliferative potential and invasiveness of pancreatic cancer cells [18].

Hepatocellular carcinoma

Up-regulation of LINC01133 in hepatocellular cancer cells has enhanced proliferation of these cells and induced aggressive phenotype in these cells. Mechanistically, LINC01133 sponges miR-199a-5p and increases expression of SNAI1, facilitating epithelial-mesenchymal transition (EMT) program in these cells. Moreover, LINC01133 has a functional interaction with Annexin A2 (ANXA2) to induce activity of ANXA2/STAT3 axis [19].

Lung cancer

LINC01133 silencing has been shown to decrease proliferative ability, migratory potential and invasiveness of non-small cell lung cancer cells and induce cell cycle arrest at G1/S stage. Mechanistically, LINC01133 has interaction with EZH2 and LSD1 to recruit these proteins to the promoter regions of KLF2, P21 or E-cadherin promoters to suppress their transcription [20].

Fig. 1
figure 1

Oncogenic roles of LINC01133 in cancers. Detailed information about mechanism of involvement of LINC01133 in these cancers is provided in Table 1. ↑ shows up-regulation. ┴ shows inhibitory effect

Full size image

Gastrointestinal cancers

LINC01133 has been shown to be down-regulated in gastric cancer cell lines. LINC01133 silencing has enhanced proliferation and migration, and induced the EMT program in gastric cancer cells, while its up-regulation has induced opposite impact. Based on the bioinformatics analyses and luciferase assay, miR-106a-3p has been found to be directly targeted by LINC01133. Mechanistically, miR-106a-3p can target adenomatous polyposis coli (APC) gene and decrease its expression. Taken together, LINC01133/miR-106a-3p has been found as a functional axis in suppression of EMT and metastasis through decreasing activity of the Wnt/β-catenin pathway via affecting APC levels [21]. Another study has shown that LINC01133 can up-regulate SST via binding to miR-576-5p. Up-regulation miR-576-5p or inhibition of SST has upturned the biological effects of LINC01133 in gastric cancer cells. Thus, LINC01133 up-regulation can suppress development of gastric cancer through decreasing expression of miR-576-5p and enhancing SST levels [22].

Fig. 2
figure 2

Tumor suppressor roles of LINC01133 in cancers. Detailed information about mechanism of involvement of LINC01133 in these cancers is provided in Table 1. ↑ shows up-regulation.┴ shows inhibitory effect

Full size image
Table 1 Expression of LINC01133 in cell lines
Full size table

Animal studies

Up-regulation of LINC01133 hepatocellular cancer cells has enhanced growth of hepatocellular carcinoma and lung metastasis in animal models, while its silencing has led to opposite effects [19]. An experiment in animal model of epithelial ovarian cancer has shown that up-regulation of this lncRNA has enhanced the metastatic ability of cells [14]. However, another study has reported enhancement of tumor weigh and volume as well as increase in metastasis following LINC01133 silencing [15].

Up-regulation of LINC01133 has reduced progression and metastasis of gastric cancer cells [21]. Similarly, experiments in an animal model of breast cancer have revealed that down-regulation of LINC01133 enhances the metastatic ability of malignant cells [25]. In order to assess the impact of LINC01133 in inhibition of colorectal cancer cells metastasis in vivo, Kong et al. have injected LINC01133-silenced HT29 cells into NOD/SCID mice. They have reported higher metastasis in the LINC01133 silenced group compared with the control group [34] (Table 2).

Table 2 Function of LINC01133 in animal models
Full size table

Human studies

Expression of LINC01133 has been shown to be down-regulated in clinical samples obtained from gastric cancer patients in correlation with progression of gastric cancer and metastasis [21]. Similar results have been obtained from expression assays in nasopharyngeal cancer [26], oral [32]/esophageal squamous cell carcinoma [37] and colorectal cancer [38] (Table 3).

Through analysis of whole genome sequencing data of hepatocellular cancer samples and matched noncancerous specimens, Yin et al. have reported increased in genomic copy numbers of LINC01133 in cancerous samples in correlation with up-regulation of LINC01133 and poor prognosis of affected individuals [19]. Similarly, assessment of expression profile of cervical cancer samples in TCGA database has revealed up-regulation of LINC01133 levels in these samples [24]. Another study has confirmed up-regulation of LINC01133 in cervical cancer samples and reported association between its levels and advanced T stage and negative HPV infection [16]. Besides, LINC01133 has been found to be up-regulated in pancreatic cancer and osteosarcoma. Dysregulation of LINC01133 in clinical samples has been frequently associated with malignant features and poor patients’ outcome. However, different experiments in in ovarian, breast and lung cancers have reported conflicting results regarding the pattern of expression of LINC01133 in cancerous versus non-cancerous samples (Table 3).

Table 3 Dysregulation of LINC01133 in clinical samples
Full size table

Discussion

LINC01133 is an important lncRNA in the process of carcinogenesis. However, it can exert dissimilar roles in this process. In gastric cancer [21], nasopharyngeal cancer [26], oral [32]/esophageal squamous cell carcinoma [37] and colorectal cancer [38], it has a tumor suppressor role. On the other hand, in hepatocellular carcinoma [19], cervical cancer [16], pancreatic cancer [29] and osteosarcoma [33], LINC01133 has been demonstrated to exert oncogenic effects. Finally, in ovarian [14, 15] and breast [17, 25] data is conflicting about the role of this lncRNA. Animal studies have also revealed conflicting results regarding the oncogenic versus tumor suppressor role of LINC01133 in different tissues.

Interaction between LINC01133 and miRNAs is a well-appreciated way of contribution of this lncRNA in the carcinogenesis. miR-106a-3p, miR-576-5p, miR-495-3p, miR-205, miR-199a-5p, miR-4784, miR-30a-5p, miR-199a, miR-30b-5p, miR-216a -5p and miR-422a are the main miRNAs mediating the effects of LINC01133 in this process (reviewed in Table 1). PI3K/AKT [23], STAT3 [19], Wnt [18], mTORC1 [30] and TGF-β [34] signaling pathways have also been shown to be affected by LINC01133. Notably, LINC01133 can affect EMT process in liver, gastric, colorectal, cervical and nasopharyngeal cancers. Thus, dysregulation of this lncRNA can enhance metastatic ability of cancer cells.

LINC01133 levels have been used to predict prognosis of cancer in different tissues (reviewed in Table 3). Dysregulation of LINC01133 has been found to affect clinical outcomes in different studies. However, since it can exert dissimilar roles in different tissues, the impact of LINC01133 down-/up-regulation on clinical outcome depends on the tissue origin.

Data about the mechanisms of dysregulation of LINC01133 in cancer is scarce. However, the presence of CNVs has been shown to affect its expression [19]. Moreover, there is no clear elucidation for tissue-specific effects of this lncRNA in the carcinogenesis. Based on the presence of conflicting results about the role of LINC01133 in the evolution of cancer, therapeutic targeting of this lncRNA should be considered with caution. Moreover, it is necessary to design novel methods for specific delivery of LINC01133-targeting therapeutic modalities to target tissues.

Availability of data and materials

The analyzed data sets generated during the study are available from the corresponding author on reasonable request.

References

  1. Qian Y, Shi L, Luo Z. Long non-coding RNAs in cancer: implications for diagnosis, prognosis, and therapy. Front Med. 2020;7:612393

    Article  Google Scholar 

  2. Wang KC, Chang HY. Molecular mechanisms of long noncoding RNAs. Mol Cell. 2011;43(6):904–14.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Quinn JJ, Chang HY. Unique features of long non-coding RNA biogenesis and function. Nat Rev Genet. 2016;17(1):47–62.

    Article  CAS  PubMed  Google Scholar 

  4. Lai F, Orom UA, Cesaroni M, Beringer M, Taatjes DJ, Blobel GA, et al. Activating RNAs associate with mediator to enhance chromatin architecture and transcription. Nature. 2013;494(7438):497–501.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Khalil AM, Guttman M, Huarte M, Garber M, Raj A, Morales DR, et al. Many human large intergenic noncoding RNAs associate with chromatin-modifying complexes and affect gene expression. Proc Natl Acad Sci. 2009;106(28):11667–72.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Jarroux J, Morillon A, Pinskaya M. History, discovery, and classification of lncRNAs. Long non coding RNA biology. Adv Exp Med Biol. 2017. https://doi.org/10.1007/978-981-10-5203-3_1.

    Article  PubMed  Google Scholar 

  7. Nikpayam E, Tasharrofi B, Sarrafzadeh S, Ghafouri-Fard S. The role of long non-coding RNAs in ovarian cancer. Iran Biomed J. 2017;21(1):3.

    Article  PubMed  PubMed Central  Google Scholar 

  8. Tsai M-C, Spitale RC, Chang HY. Long intergenic noncoding RNAs: new links in cancer progression. Cancer Res. 2011;71(1):3–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Gupta RA, Shah N, Wang KC, Kim J, Horlings HM, Wong DJ, 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 

  10. Li G, Wang C, Wang Y, Xu B, Zhang W. LINC00312 represses proliferation and metastasis of colorectal cancer cells by regulation of miR-21. J Cell Mol Med. 2018;22(11):5565–72.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Liao M, Li B, Zhang S, Liu Q, Liao W, Xie W, et al. Relationship between LINC00341 expression and cancer prognosis. Oncotarget. 2017;8(9):15283–93.

    Article  PubMed  PubMed Central  Google Scholar 

  12. Xiu B, Chi Y, Liu L, Chi W, Zhang Q, Chen J, et al. LINC02273 drives breast cancer metastasis by epigenetically increasing AGR2 transcription. Mol Cancer. 2019;18(1):1–20.

    Article  CAS  Google Scholar 

  13. Guttman M, Amit I, Garber M, French C, Lin MF, Feldser D, et al. Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals. Nature. 2009;458(7235):223–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Liu S, Xi X. LINC01133 contribute to epithelial ovarian cancer metastasis by regulating miR-495-3p/TPD52 axis. Biochem Biophys Res Commun. 2020;533(4):1088–94.

    Article  CAS  PubMed  Google Scholar 

  15. Liu M, Shen C, Wang C. Long noncoding RNA LINC01133 confers tumor-suppressive functions in ovarian cancer by regulating leucine-rich repeat kinase 2 as an miR-205 sponge. Am J Pathol. 2019;189(11):2323–39.

    Article  CAS  PubMed  Google Scholar 

  16. Zhang D, Zhang Y, Sun X. LINC01133 promotes the progression of cervical cancer via regulating miR-30a‐5p/FOXD1. Asia Pac J Clin Oncol. 2021;17(3):253–63.

    Article  PubMed  Google Scholar 

  17. Tu Z, Schmöllerl J, Cuiffo BG, Karnoub AE. Microenvironmental regulation of long noncoding RNA LINC01133 promotes cancer stem cell-like phenotypic traits in triple‐negative breast cancers. Stem Cells. 2019;37(10):1281–92.

    Article  CAS  PubMed  Google Scholar 

  18. Weng Y-C, Ma J, Zhang J, Wang J-C. Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway. Cancer Biol Ther. 2019;20(3):368–80.

    Article  CAS  PubMed  Google Scholar 

  19. Yin D, Hu ZQ, Luo CB, Wang XY, Xin HY, Sun RQ, et al. LINC01133 promotes hepatocellular carcinoma progression by sponging miR-199a‐5p and activating annexin A2. Clin Trans Med. 2021;11(5):e409.

    Article  CAS  Google Scholar 

  20. Zang C, Nie F-q, Wang Q, Sun M, Li W, He J, et al. Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. Oncotarget. 2016;7(10):11696.

    Article  PubMed  PubMed Central  Google Scholar 

  21. Yang X-Z, Cheng T-T, He Q-J, Lei Z-Y, Chi J, Tang Z, et al. LINC01133 as ceRNA inhibits gastric cancer progression by sponging miR-106a-3p to regulate APC expression and the Wnt/β-catenin pathway. Mol Cancer. 2018;17(1):1–15.

    Google Scholar 

  22. Zhang L, Pan K, Zuo Z, Ye F, Cao D, Peng Y, et al. LINC01133 hampers the development of gastric cancer through increasing somatostatin via binding to microRNA-576-5p. Epigenomics. 2021;13(15):1205–19.

    Article  CAS  PubMed  Google Scholar 

  23. Zheng YF, Zhang XY, Bu YZ. LINC01133 aggravates the progression of hepatocellular carcinoma by activating the PI3K/AKT pathway. J Cell Biochem. 2019;120(3):4172–9.

    Article  CAS  PubMed  Google Scholar 

  24. Feng Y, Qu L, Wang X, Liu C. LINC01133 promotes the progression of cervical cancer by sponging miR-4784 to up-regulate AHDC1. Cancer Biol Ther. 2019;20(12):1453–61.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Song Z, Zhang X, Lin Y, Wei Y, Liang S, Dong C. LINC01133 inhibits breast cancer invasion and metastasis by negatively regulating SOX4 expression through EZH2. J Cell Mol Med. 2019;23(11):7554–65.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Zhang W, Du M, Wang T, Chen W, Wu J, Li Q, et al. Long non-coding RNA LINC01133 mediates nasopharyngeal carcinoma tumorigenesis by binding to YBX1. Am J Cancer Res. 2019;9(4):779.

    CAS  PubMed  PubMed Central  Google Scholar 

  27. Zhai X, Wu Y, Wang Z, Zhao D, Li H, Chong T, et al. Long noncoding RNA LINC01133 promotes the malignant behaviors of renal cell carcinoma by regulating the miR-30b-5p/Rab3D axis. Cell Transplant. 2020;29:0963689720964413.

    Article  PubMed Central  Google Scholar 

  28. Yang W, Yue Y, Yin F, Qi Z, Guo R, Xu Y. LINC01133 and LINC01243 are positively correlated with endometrial carcinoma pathogenesis. Arch Gynecol Obstet. 2021;303(1):207–15.

    Article  CAS  PubMed  Google Scholar 

  29. Huang C-S, Chu J, Zhu X-X, Li J-H, Huang X-T, Cai J-P, et al. The C/EBPβ-LINC01133 axis promotes cell proliferation in pancreatic ductal adenocarcinoma through upregulation of CCNG1. Cancer Lett. 2018;421:63–72.

    Article  CAS  PubMed  Google Scholar 

  30. Zhang J, Gao S, Zhang Y, Yi H, Xu M, Xu J, et al. MiR-216a-5p inhibits tumorigenesis in pancreatic cancer by targeting TPT1/mTORC1 and is mediated by LINC01133. Int J Biol Sci. 2020;16(14):2612.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Liu Y, Tang T, Yang X, Qin P, Wang P, Zhang H, et al. Tumor-derived exosomal long noncoding RNA LINC01133, regulated by periostin, contributes to pancreatic ductal adenocarcinoma epithelial-mesenchymal transition through the Wnt/β-catenin pathway by silencing AXIN2. Oncogene. 2021;40(17):3164–79.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Kong J, Sun W, Zhu W, Liu C, Zhang H, Wang H. Long noncoding RNA LINC01133 inhibits oral squamous cell carcinoma metastasis through a feedback regulation loop with GDF15. J Surg Oncol. 2018;118(8):1326–34.

    Article  CAS  PubMed  Google Scholar 

  33. Zeng H-F, Qiu H-Y, Feng F-B. Long noncoding RNA LINC01133 functions as an miR-422a sponge to aggravate the tumorigenesis of human osteosarcoma. Oncol Res. 2018;26(3):335.

    Article  PubMed  PubMed Central  Google Scholar 

  34. Kong J, Sun W, Li C, Wan L, Wang S, Wu Y, et al. Long non-coding RNA LINC01133 inhibits epithelial–mesenchymal transition and metastasis in colorectal cancer by interacting with SRSF6. Cancer Lett. 2016;380(2):476–84.

    Article  CAS  PubMed  Google Scholar 

  35. Zhang J, Zhu N, Chen X. A novel long noncoding RNA LINC01133 is upregulated in lung squamous cell cancer and predicts survival. Tumor Biology. 2015;36(10):7465–71.

    Article  CAS  PubMed  Google Scholar 

  36. Yang H, Qu H, Huang H, Mu Z, Mao M, Xie Q, et al. Exosomes-mediated transfer of long noncoding RNA LINC01133 represses bladder cancer progression via regulating the Wnt signaling pathway. Cell Biol Int. 2021. https://doi.org/10.1002/cbin.11590.

    Article  PubMed  PubMed Central  Google Scholar 

  37. Yang X-Z, He Q-J, Cheng T-T, Chi J, Lei Z-Y, Tang Z, et al. Predictive value of LINC01133 for unfavorable prognosis was impacted by alcohol in esophageal squamous cell carcinoma. Cell Physiol Biochem. 2018;48(1):251–62.

    Article  CAS  PubMed  Google Scholar 

  38. Zhang J, Li A, Wei N. Downregulation of long non-coding RNA LINC01133 is predictive of poor prognosis in colorectal cancer patients. Eur Rev Med Pharmacol Sci. 2017;21(9):2103–7.

    PubMed  Google Scholar 

  39. Foroughi K, Amini M, Atashi A, Mahmoodzadeh H, Hamann U, Manoochehri M. Tissue-specific down-regulation of the long non-coding RNAs PCAT18 and LINC01133 in gastric cancer development. Int J Mol Sci. 2018;19(12):3881.

    Article  PubMed Central  CAS  Google Scholar 

  40. Ding S, Huang X, Zhu J, Xu B, Xu L, Gu D, et al. ADH7, miR–3065 and LINC01133 are associated with cervical cancer progression in different age groups. Oncol Lett. 2020;19(3):2326–38.

    CAS  PubMed  PubMed Central  Google Scholar 

  41. Wang W-J, Di Wang MZ, Sun X-J, Li Y, Lin H, Che Y-Q, et al. Serum lncRNAs (CCAT2, LINC01133, LINC00511) with squamous cell carcinoma antigen panel as novel non-invasive biomarkers for detection of cervical squamous carcinoma. Cancer Manag Res. 2020;12:9495.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Mehrpour Layeghi S, Arabpour M, Shakoori A, Naghizadeh MM, Mansoori Y, Tavakkoly Bazzaz J, et al. Expression profiles and functional prediction of long non-coding RNAs LINC01133, ZEB1-AS1 and ABHD11-AS1 in the luminal subtype of breast cancer. J Transl Med. 2021;19(1):1–17.

    Article  CAS  Google Scholar 

  43. Giulietti M, Righetti A, Principato G, Piva F. LncRNA co-expression network analysis reveals novel biomarkers for pancreatic cancer. Carcinogenesis. 2018;39(8):1016–25.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

This study was financially supported by Grant from Medical School of Shahid Beheshti University of Medical Sciences.

Funding

Open Access funding enabled and organized by Projekt DEAL.

Author information

Authors and Affiliations

  1. Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Soudeh Ghafouri-Fard

  2. Phytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Tayyebeh Khoshbakht

  3. Department of Pharmacognosy, College of Pharmacy, Hawler Medical University, Kurdistan Region, Erbil, Iraq

    Bashdar Mahmud Hussen

  4. Institute of Human Genetics, Jena University Hospital, Jena, Germany

    Mohammad Taheri

  5. Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Mohammad Taheri

  6. Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Majid Mokhtari

Authors
  1. Soudeh Ghafouri-Fard
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Tayyebeh Khoshbakht
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Bashdar Mahmud Hussen
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Mohammad Taheri
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Majid Mokhtari
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

SGF wrote the manuscript and revised it. MT supervised and designed the study. TK, MM and BMH collected the data and designed the figures and tables. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Mohammad Taheri or Majid Mokhtari.

Ethics declarations

Ethics approval and consent to participant

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent forms were obtained from all study participants. The study protocol was approved by the ethical committee of Shahid Beheshti University of Medical Sciences. All methods were performed in accordance with the relevant guidelines and regulations.

Consent of publication

Not applicable.

Competing interests

The authors declare they have no conflict of interest.

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

Ghafouri-Fard, S., Khoshbakht, T., Hussen, B.M. et al. A review on the role of LINC01133 in cancers. Cancer Cell Int 22, 270 (2022). https://doi.org/10.1186/s12935-022-02690-z

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12935-022-02690-z

Keywords

Cancer Cell International

ISSN: 1475-2867

Contact us