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

OncoTargets and Therapy. 2016;2016(Issue 1):1011-1021

 

Journal Homepage

Journal Title: OncoTargets and Therapy

ISSN: 1178-6930 (Online)

Publisher: Dove Medical Press

LCC Subject Category: Medicine: Internal medicine: Neoplasms. Tumors. Oncology. Including cancer and carcinogens

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS

Ge Y
Cao XK
Wang DL
Sun W
Sun HL
Han B
Cui JP
Liu BL

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 16 weeks

 

Abstract | Full Text

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