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miR-135a acts as a tumor suppressor in gastric cancer in part by targeting KIFC1

Authors Zhang C, Chen X, Chen X, Wang X, Ji A, Jiang L, Sang F, Li F

Received 3 February 2016

Accepted for publication 27 April 2016

Published 15 June 2016 Volume 2016:9 Pages 3555—3563

DOI https://doi.org/10.2147/OTT.S105736

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Manfred Beleut

Peer reviewer comments 4

Editor who approved publication: Dr William Cho


Chuanlei Zhang,1 Xiaoqi Chen,1 Xinju Chen,1 Xinting Wang,1 Aiying Ji,1 Lifeng Jiang,2 Feng Sang,3 Fucheng Li4

1Department of Digestive Diseases, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, 2Department of Chinese Traditional and Western Medicine, Henan Cancer Hospital, Affiliated Cancer Hospital of Zhengzhou University, 3Department of Acquired Immune Deficiency Syndrome Treatment and Research Center, Key Laboratory of Viral Diseases Prevention and Treatment of Traditional Chinese Medicine of Henan Province, 4The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, People’s Republic of China

Abstract: miR-135a was downregulated in the majority of human primary gastric cancer (GC) tissues and GC cell lines. Kinesin family member C1 (KIFC1) was significantly upregulated in GC tissues and cell lines and promoted GC development and progression. We searched for miR-135a targets by using MiRanda, TargetScan, and PicTar tools, and found that KIFC1 was a potential target of miR-135a. Based on these findings, we speculated that miR-135a might target KIFC1 to inhibit GC growth. We determined the expression of miR-135a and KIFC1 by quantitative real-time polymerase chain reaction and Western blot assays, respectively, and found downregulation of miR-135a and upregulation of KIFC1 in GC tissues and cell lines. Cell proliferation and apoptosis assays showed that knockdown of KIFC1 inhibited proliferation and promoted apoptosis of GC cells, and miR-135a mimics had similar effects on GC cell proliferation and apoptosis. Furthermore, we verified that KIFC1 was a direct target of miR-135a, which confirmed our speculation that the functional effect of miR-135a on GC cells, at least, in part, depends on KIFC1. These findings suggest that miR-135a has an important role in the suppression of GC and presents a novel mechanism of miRNA-mediated KIFC1 expression in cancer cells.

Keywords: gastric cancer, miR-135a, kinesin family member C1, proliferation, apoptosis

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