Table 1 miR-630 in cancers (ANCT adjacent non-cancerous tissue, GEO gene expression omnibus)
From: The importance of miRNA-630 in human diseases with an especial focus on cancers
Type of cancer | Expression pattern | Samples | Cell lines | Downstream targets | Other related molecules and pathways | Function | Refs. |
|---|---|---|---|---|---|---|---|
Renal cell carcinoma (RCC) | Up | – | 786-O, ACHN, Caki-1, Caki-2 and HK-2 | – | – | Inhibition of miR-630 could suppress tumorigenesis | [8] |
Multiple myeloma (MM) | Up | Plasma from 40 MM patients and 20 control subjects | – | – | – | miR-630 was categorized as a differentially expressed miRNA between MM patients and healthy subjects | [24] |
Colorectal cancer (CRC) | – | – | HCT116 | P27, BAX and caspase-3, p-AKT and BCL2 | AKT pathway | Overexpression of miR-630 via inhibiting of P27, BAX and, caspase-3 and enhancing p-AKT and BCL2 could increase cell proliferation and immortality. Suppression of it could have an opposite effect | [9] |
Acute lymphoblastic leukemia (ALL) | – | – | Jurkat cells | P53, P21, and BCL2 | P53 pathway | Overexpression of miR-630 by suppressing P53 and p21 and via bcl2 enhancement could lead to the growth of cancer cells and inhibition of the apoptosis process | [10] |
Ovarian Cancer (OC) | Up | 30 ovarian cancer tissues, 30 normal ovarian tissues/mice | SKOV3 | KLF6 | – | Overexpression of miR-630 could enhance tumorigenesis | [11] |
Prostate cancer (PCa) | Up | 10 pairs of PCa Tumors and ANCTs from young men | – | – | – | miR-630 up-regulated in young men tumor tissues than their normal adjacent tissues | [13] |
Hepatocellular carcinoma (HCC) | Up | 42 pairs of tumors and ANCTs | SMMC-7721, Hep3B, HepG2, HCCLM3,LO2 and HL-7702 | AFP | – | A direct correlation between AFP level and miR-630 expression could be observed | [14] |
– | – | QSG7701, HL7702, HCCLM3, MHCC97H, MHCC97L, SMMC-7721, HLF, Bel7402, HepG2, Hep3B and Huh7 | Slug, E-cadherin, N-cadherin, and vimentin | TGF-β-ERK/SP1 and JNK/c-Jun | miR-630 could diminish cell migration, invasion, and EMT and also afford apoptosis. TGF-β by ERK/SP1 and JNK/c-Jun pathways could inhibit miR-630 | [15] | |
Pancreatic cancer (PC) | – | GEO database | – | NTS, CDH2, GRIA2 | PI3K/AKT | miR-630 could promote apoptosis by affecting PI3K/AKT pathway | [25] |
Non-small cell lung cancer (NSCLC) | Down | 22 pairs of NSCLC tissues and ANCTs | NCI-H23, A549, H157, H1299 and 16HBE | LMO3 | – | The expression level of miR-630 could have an opposite correlation with LMO3, and its overexpression could suppress tumorigenesis | [17] |
Cervical cancer (CC) | Down | 10 pairs of cervical tumors and ANCTs | Caski, Ms751, Hela and Siha | Vimentin, N-cadherin, E-cadherin, Snail, Zeb1 and Zeb2 | E6/E7-p53 signaling pathway | E6/E7 by inhibition of P53 could suppress miR-630 that provokes invasion, migration, and EMT of cancer cells | [26] |
Down | Mice | Caski, HeLa, C‐33A, SiHa, SW756, and HcerEpic | YAP1 | LncRNA NOC2L‐4.1 | NOC2L‐4.1 by regulation of miR‐630/YAP1 axis could promote cell multiplication and migration. NOC2L‐4.1 and YAP1 had an inverse correlation with miR-630 | [27] | |
Breast cancer (BC) | Down | 43 pairs of tumor tissues and ANCTs | MDA-MB-231-luc-D3H2LN, MCF-10A, MDA-MB-231, MDA-MB-468, MDA-MB-435S, BT-549, BT-474, SK-BR-3, HCC1937, MCF7, and HEK293T | MTDH | – | Over-expression of miR-630 could prevent cell migration, invasion, colony formation, and pulmonary metastasis | [28] |
Gastric cancer (GC) | Down | Blood, tumor tissue and ANCTs from 131 patients/blood sample from 116 healthy persons | SGC-7901 | SOX4, p21, p27, MMP2, and MMP9 | – | Over-expression of miR-630 and as a result decreased expression of SOX4 could reduce proliferation and invasion of cells | [18] |
Up | 167 pairs of tumors and ANCTs | AGS, MKN28, MKN45, BGC823, MGC803, SGC7901, and GES1 | – | CircRNA-100269 | miR-630 as a target of circRNA-100269 could have a negative correlation with this circular RNA. So, it could reverse the inhibitory effects of circRNA-100269 | [19] | |
– | – | SGC-7901 | FoxM1, Ecadherin, vimentin, GTP-Rac1, p-PI3K, and p-AKT | Ras/PI3K/AKT | miR-630 could cause migration, invasion, and EMT decline | [20] | |
Nasopharyngeal carcinoma (NPC) | Up | Plasma sample from 55 NPC patients and 45 controls | – | – | – | miR-630 could be considered as a new biomarker in NPC | [22] |
– | – | NP69, CNE2, CNE1, and HONE1 | EZH2, E-cadherin | H19 | H19 as a sponge for miR-630 could regulate EZH2 and led to cell invasion | [23] | |
Osteosarcoma | Down | 147 pairs of tumor tissues and ANCTs | Saos-2, U2OS, MG63, HOS and hFOB1.19 | PSMC2, N-cadherin and vimentin | – | miR-630 as an upstream tumor suppressor factor of PSMC2 could inhibit tumor characteristics | [29] |
Papillary thyroid carcinoma (PTC) | Down | 47 pairs of PTC tissues and ANCTs/GEO database | Nthy-ori3-1, SW1736, 8505C and TPC-1 | Caspase3, caspase9, vimentin, N-cadherin, p-JAK2 and p-STAT3 | JAK2/STAT3 | Up-regulation of miR-630 could inhibit proliferation, invasion, and migration processes and could cause apoptosis | [30] |
Esophageal cancer | Down | Peripheral blood from 58 EC patients and 60 controls | KYSE-150, KYSE-450, ECA109 and HEEC | – | – | miR-630 induction in malignant cells could inhibit migration and invasion | [31] |
Esophageal squamous cell carcinoma (ESCC) | Down | 44 pairs of tumors and ANCTs/mice | Eca109, EC9706, TE1, Kyse-30, Kyse-70 and HEEC | E-cadherin, β-catenin N-cadherin, slug, and vimentin | – | miR-630 upregulation could suppress proliferation, metastasis, EMT, and invasion of cells | [32] |