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Lipopolysaccharide-induced α-catenin downregulation enhances the motility of human colorectal cancer cells in an NF-κB signaling-dependent manner

Authors Cheng G, Yang S, Zhang G, Xu Y, Liu X, Sun W, Zhu L

Received 6 October 2016

Accepted for publication 18 November 2016

Published 14 December 2016 Volume 2016:9 Pages 7563—7571


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Chang Liu

Peer reviewer comments 2

Editor who approved publication: Dr Carlos E Vigil

Guoping Cheng,1,2 Shifeng Yang,1 Gu Zhang,1 Yanxia Xu,3 Xiaoling Liu,3 Wenyong Sun,1,2 Liang Zhu3

1Department of Pathology, Zhejiang Cancer Hospital, 2Cancer Research Institute, Zhejiang Cancer Hospital and Key laboratory Diagnosis and Treatment Technology on Thoracic Oncology of Zhejiang Province, 3School of Medicine, Hangzhou Normal University, Hangzhou, Zhejiang, People’s Republic of China

α-Catenin is an important molecule involved in the maintenance of cell–cell adhesion and a prognostic marker in cancer since its expression is essential for preventing cancer metastasis. However, the mechanism that leads to the downregulation of α-catenin in cancer progression remains unclear. The present study revealed that lipopolysaccharide (LPS)-induced NF-κB signaling activation suppressed α-catenin expression and motility in SW620 colorectal cancer (CRC) cells, using real-time polymerase chain reaction, Western blotting, and transwell migration assays. LPS treatment reduced both the mRNA and protein expression of α-catenin and thereby enhanced cell motility. Conversely, incubating cells with an NF-κB inhibitor disrupted these effects. Furthermore, the ectopic expression of p65 alone mimicked the effects of LPS stimulation. In CRC tissues, the presence of enteric bacterial LPS-related neutrophil-enriched foci was correlated with α-catenin downregulation. Collectively, these findings suggest that LPS-induced NF-κB signaling is related to α-catenin suppression and enhanced cell motility in CRC. Therefore, NF-κB is a novel potential therapeutic target for CRC metastasis.

lipopolysaccharide, colorectal neoplasms, α-catenin, neoplasm metastasis

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