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Expression of microRNA-30c via lentivirus vector inhibits the proliferation and enhances the sensitivity of highly aggressive ccRCC Caki-1 cells to anticancer agents

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


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

Honglin Yang,1,* Erlin Song,2,3,* Guorong Shen,1 Tonghua Zhu,1 Tingwang Jiang,4 Hao Shen,1 Liping Niu,1 Biao Wang,1 Zhaoyang Lu,5 Jianping Qian4

1Department of Laboratory Medicine, The first people's Hospital of Wujiang District, Suzhou, 2Department of Urinary Surgery, The First Affiliated Hospital of Harbin Medical University, 3Key Laboratory of Cardiovascular Medicine Research, Harbin Medical University, Ministry of Education, Harbin, 4Changshu Institution for Laboratory Medicine, Changshu, 5Department of Ultrasound Diagnosis, The first people's Hospital of Wujiang District, Suzhou, People's Republic of China

*These authors contributed equally to this work

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

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