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miR-7 inhibits colorectal cancer cell proliferation and induces apoptosis by targeting XRCC2

Authors Xu K, Chen Z, Qin C, Song X

Received 18 December 2013

Accepted for publication 16 January 2014

Published 20 February 2014 Volume 2014:7 Pages 325—332


Checked for plagiarism Yes

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Peer reviewer comments 3

Kaiwu Xu, Zhihui Chen, Changjiang Qin, Xinming Song

Gastrointestinal and Pancreatic Surgery Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, People’s Republic of China

Background: Analysis using publicly available algorithms predicts that X-ray repair complementing defective repair in Chinese hamster cells 2 (XRCC2), a key component in the homologous recombination repair pathway, is a potential target of micro-ribonucleic acid-7 (miR-7). Some studies have shown that both miR-7 and XRCC2 are associated with cancer development. For this purpose, we searched for the possible relationship between miR-7 and XRCC2 in the development of colorectal cancer (CRC).
Methods: miR-7 expression was assessed in CRC specimens and cell lines using real-time polymerase chain reaction (PCR). Luciferase reporter assay was used to confirm the target associations. The effect of miR-7 on cell proliferation and apoptosis was confirmed in vitro by the methylthiazol tetrazolium (MTT) assay, colony formation assay, and flow cytometry. Gene and protein expression were examined using real time PCR and western blotting, respectively.
Results: miR-7 was downregulated in CRC specimens and cell lines, and targeted the 3' untranslated region of XRCC2. miR-7 overexpression reduced cyclin D1 expression and increased p21, caspase-3, and BAX expression, which subsequently inhibited CRC cell proliferation and induced CRC cell apoptosis. However, XRCC2 can repress the inhibitory effects of miR-7 on proliferation.
Conclusion: Our findings suggest that miR-7 plays a protective role by inhibiting proliferation and increasing apoptosis of CRC cells. It may identify new targets for anti-cancer treatment.

Keywords: MiRNA, DNA, overexpression, downregulated

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