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miR-136 targets MIEN1 and involves the metastasis of colon cancer by suppressing epithelial-to-mesenchymal transition

Authors Ren H, Qi Y, Yin X, Gao J

Received 22 May 2016

Accepted for publication 15 September 2016

Published 22 December 2017 Volume 2018:11 Pages 67—74

DOI https://doi.org/10.2147/OTT.S113359

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Akshita Wason

Peer reviewer comments 3

Editor who approved publication: Dr XuYu Yang


Haipeng Ren,1 Yuanling Qi,1 Xiaoyan Yin,2 Jianfeng Gao1

1Department of Internal Medicine of Oncology, People’s Hospital of Weifang, Weifang, 2Health and Family Planning Bureau of Weifang, Shouguang, People’s Republic of China

Abstract: MIEN1 is a novel oncogene, and it involves tumor progression in various cancer types, including colon cancer. However, the definite molecular mechanisms of MIEN1 in colon cancer progression remain to be completely elucidated. In the present study, bioinformatics prediction showed that miR-136 could be an upstream regulator of MIEN1; a luciferase assay and Western blot assay revealed that miR-136 negatively regulates MIEN1 expression via directly targeting its 3'-untranslated region sequence. Moreover, a functional assay using wound healing and transwell invasion showed that overexpressed miR-136 inhibited cell migration and invasion, and overexpression of MIEN1 partly rescued the above-mentioned effects of miR-136 in colon cancer cells. Additionally, a clinical sample assay showed that miR-136 expression was generally downregulated in colon cancer tissue, which was inversely correlated with MIEN1 expression. Furthermore, we found that miR-136 suppressed the Akt/NF-κB signaling pathway and epithelial-to-mesenchymal transition in colon cancer. These results suggest that miR-136, as a tumor suppressor, acts in tumor metastasis by suppressing MIEN1 expression in colon cancer, providing a novel target for the treatment of colon cancer.

Keywords: colon cancer, miR-136, MIEN1, migration, invasion

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