已发表论文

microRNA-30c 通过慢病毒载体的表达抑制增殖,并增强具有高度侵略性的 ccRCC Caki-1 细胞对抗癌剂的敏感性

 

Authors Yang HL, Song EL, Shen GR, Zhu TH, Jiang TW, Shen H, Niu LP, Wang B, Lu ZY, Qian JP

Received 25 June 2016

Accepted for publication 29 November 2016

Published 2 February 2017 Volume 2017:10 Pages 579—590

DOI https://doi.org/10.2147/OTT.S115791

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Chang Liu

Peer reviewer comments 4

Editor who approved publication: Dr Tohru Yamada

Abstract: The clear cell renal cell carcinoma (ccRCC) is one of the most fatal urologic tumors, and the prognosis remains very poor for advanced or metastatic ccRCC. This study reveals the roles of microRNA (miR)-30c in regulating a highly aggressive ccRCC cell line proliferation by targeting MTA-1, which is a key mediator for human cancer metastasis. Results from quantitative real-time polymerase chain reaction showed that the expression of MTA-1, the target of miR-30c, was significantly higher in metastatic ccRCC specimens than in nonmetastatic ccRCC or nontumor specimens. Accordingly, endogenous miR-30c is at a much lower level in highly aggressive ccRCC Caki-1 cells than nontumor or ccRCC cell lines. Expression of miR-30c via lentivirus vector inhibits the proliferation, anchorage-independent growth, in vitro invasion or migration, or in vivo growth of Caki-1 cells by repressing MTA-1 protein expression. miR-30c also enhances the sensitivity of Caki-1 cells to anticancer agents, including sorafenib and paclitaxel. These data reveal the potential application of miR-30c and that its targeting gene, MTA-1, would be a potential target in metastatic ccRCC treatment.
Keywords: ccRCC, miR-30c, MTA-1, sorafenib, paclitaxel, Caki-1