| Note | |
| | |
| Entity | Tumor cell proliferation |
| Note | Abnormal expression of miR-200a was reported in various tumors, including human breast cancer, gastric carcinoma, endometrial adenocarcinoma, gliomas, and colorectal carcinoma. MiR-429 could inhibit cell growth and induce apoptosis by directly targeting ONECUT2 in colorectal carcinoma and targeting BCL2 in esophageal carcinoma (Sun, Shen et al. 2014). Also, MiR-429 could induce apoptosis and suppress invasion by targeting BCL2 and SP1 in esophageal carcinoma (Wang, Li et al. 2013). However, miR-429 was also showed its anti-apoptosis function in colorectal cancer by targeting SOX2 (Li, Du et al. 2013). |
| | |
| | |
| Entity | Tumor cells invasion and cancer metastasis |
| Note | Members of miR-200 family showed vital roles in tumor cells invasion and cancer metastasis. As to miR-429, studies demonstrated it could repress tumor cell invasion and cancer metastasis by targeting ONECUT2 and SP1 in different tumors (Sun, Shen et al. 2014; Wang, Li et al. 2013). |
| | |
| | |
| Entity | Repression of epithelial-mesenchymal transition (EMT) |
| Note | EMT is an important feature of tumor cells. Tumor cells underwent EMT showed more invasion and metastatic properties. Studies demonstrated members of miR-200 family could directly target ZEB1 and ZEB2 and could be regulated as a feedback loop during EMT. Ectopic over-expression of miR-429 induces mesenchymal-to-epithelial transition (MET) in metastasizing ovarian cancer cells (Chen, Wang et al. 2011). In colorectal carcinoma cells, miR-429 could regulate EMT-related markers such as ZEB2, Vimentin, SNAI2 (SLUG) and SNAI1 (SNAIL) by targeting ONECUT2 (Sun, Shen et al. 2014). |
| | |
| | |
| Entity | Chemoresistance |
| Note | Cancer stem cells showed highly resistance to chemotherapy which make relapse of tumor. It was found that over-expression of miR-429 could increase drug sensitivity in metastasizing ovarian (Wang, Mezencev et al. 2014). However, it was reported that miR-429 was highly expressed in hepatocellular carcinoma tissues and enrichment of miR-429 in liver tumour-initiating cells with EPCAM expression would contributed to hepatocyte self-renewal, malignant proliferation, chemoresistance and tumorigenicity (Li, Tang et al. 2014). |
| | |
| Overexpression of miR-429 induces mesenchymal-to-epithelial transition (MET) in metastatic ovarian cancer cells |
| Chen J, Wang L, Matyunina LV, Hill CG, McDonald JF |
| Gynecol Oncol 2011 Apr;121(1):200-5 |
| PMID 21277012 |
| |
| MiR-429 is an independent prognostic factor in colorectal cancer and exerts its anti-apoptotic function by targeting SOX2 |
| Li J, Du L, Yang Y, Wang C, Liu H, Wang L, Zhang X, Li W, Zheng G, Dong Z |
| Cancer Lett 2013 Feb 1;329(1):84-90 |
| PMID 23111103 |
| |
| Epigenetic modification of MiR-429 promotes liver tumour-initiating cell properties by targeting Rb binding protein 4 |
| Li L, Tang J, Zhang B, Yang W, LiuGao M, Wang R, Tan Y, Fan J, Chang Y, Fu J, Jiang F, Chen C, Yang Y, Gu J, Wu D, Guo L, Cao D, Li H, Cao G, Wu M, Zhang MQ, Chen L, Wang H |
| Gut 2015 Jan;64(1):156-67 |
| PMID 24572141 |
| |
| MiR-429 inhibits cells growth and invasion and regulates EMT-related marker genes by targeting Onecut2 in colorectal carcinoma |
| Sun Y, Shen S, Liu X, Tang H, Wang Z, Yu Z, Li X, Wu M |
| Mol Cell Biochem 2014 May;390(1-2):19-30 |
| PMID 24402783 |
| |
| Ectopic over-expression of miR-429 induces mesenchymal-to-epithelial transition (MET) and increased drug sensitivity in metastasizing ovarian cancer cells |
| Wang L, Mezencev R, Svajdler M, Benigno BB, McDonald JF |
| Gynecol Oncol 2014 Jul;134(1):96-103 |
| PMID 24802724 |
| |
| MiR-429 up-regulation induces apoptosis and suppresses invasion by targeting Bcl-2 and SP-1 in esophageal carcinoma |
| Wang Y, Li M, Zang W, Ma Y, Wang N, Li P, Wang T, Zhao G |
| Cell Oncol (Dordr) 2013 Oct;36(5):385-94 |
| PMID 23999873 |
| |
