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Overexpression of Livin promotes migration and invasion of colorectal cancer cells by induction of epithelial–mesenchymal transition via NF-κB activation

Authors Ge Y, Cao X, Wang D, Sun W, Sun H, Han B, Cui J, Liu B

Received 4 August 2015

Accepted for publication 28 November 2015

Published 29 February 2016 Volume 2016:9 Pages 1011—1021


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Faris Farassati

Yang Ge,1,2 Xiankui Cao,1 Dalu Wang,3 Wei Sun,1 Hongli Sun,1 Bing Han,1 Junpeng Cui,1 Baolin Liu1

1The Sixth Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 2Department of General Surgery, General Hospital Under the Fushun Mining Affairs Bureau, Fushun, 3The Eighth Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People’s Republic of China

Abstract: Livin is a novel member of the inhibitors of apoptosis protein family and has been implicated in the development and progression of colorectal cancer (CRC). However, the underlying mechanisms of Livin in CRC remain not fully understood. In this study, we investigated the effects of Livin expression on the proliferation and metastasis of CRC cells and also addressed its related molecular mechanism to metastasis. The expression of Livin in CRC cells (HCT116, SW480, and HT-29 cell lines) was determined by Western blot analysis. Our results show that the overexpression of Livin significantly promotes the proliferation, migration, and invasion of SW480 cells. Concurrently, the inhibition of Livin reduces the proliferation, migration, and invasion of HCT116 cells. In addition, Livin overexpression promotes the epithelial–mesenchymal transition, as evidenced by a decrease in epithelial E-cadherin expression and an increase in mesenchymal markers, including vimentin, Slug, and Snail. Furthermore, adding the NF-κB inhibitor, BAY 11-7028, or transfecting with small interfering RNA against p65 notably restores the expression level of E-cadherin and attenuates the invasive ability of Livin-overexpressing cells. Taken together, these results indicate that Livin potentiates migration and invasion of CRC cells partially through the induction of epithelial–mesenchymal transition via NF-κB activation. Livin may be a potential therapeutic target for CRC.

Keywords: Livin, colorectal cancer, migration, invasion, epithelial–mesenchymal transition, NF-κB

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