Open AccessmiR-17-3P regulates the proliferation and survival of colon cancer cells by targeting Par4
Author(s) -
Debao Lu,
Liang Tang,
Yan Zhuang,
Peng Zhao
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7863
Subject(s) - gene silencing , oncogene , microrna , cancer research , apoptosis , downregulation and upregulation , cell growth , transfection , colorectal cancer , biology , cancer , cell cycle , cell , cell culture , gene , genetics
Colorectal cancer (CRC) is a common malignancy worldwide. However, the pathogenesis by which CRC progression occurs remains to be elucidated. The present study investigated the role of miRNA (miR)‑17‑3P in the regulation of CRC cell survival. Firstly, miR‑17‑3P expression was aberrantly upregulated in human CRC tumor tissues compared with controls. Further results demonstrated that the proliferation capacity of human CRC SW480 and LoVo cells was significantly increased by an miR‑17‑3P specific mimic, and was inhibited by miR‑17‑3P silencing. Conversely, the apoptosis of human CRC cells was remarkably decreased by miR‑17‑3P mimic, and enhanced by miR‑17‑3P suppression compared with control. Additionally, it was observed that there was a potential binding site of miR‑17‑3P on the 3'‑untranslated region of Prostate apoptosis responde‑4 (Par4) and miR‑17‑3P may directly target Par4 mRNA. In human CRC cells, an miR‑17‑3P inhibitor significantly upregulated Par 4 expression, however the miR‑17‑3P mimic reduced Par4expression. Furthermore, Par4 expression exhibited an inhibitory effect on the proliferation of CRC cells transfected with miR‑17‑3P mimic, and exhibited a promoting role in the repressed apoptosis by miR‑17‑3P mimic. Inconclusion, the results of the present study demonstrated that miR‑17‑3P is important in CRC cell survival by targeting Par4, indicating a novel finding regarding human CRC progression.