Zhou D, Dong P, Li YM, Guo FC, Zhang AP, Song RZ, Zhang YM, Li ZY, Yuan D, Yang C. Overexpression of Csk-binding protein decreases growth, invasion, and migration of esophageal carcinoma cells by controlling Src activation. World J Gastroenterol 2015; 21(6): 1814-1820 [PMID: 25684946 DOI: 10.3748/wjg.v21.i6.1814]
Corresponding Author of This Article
Yu-Min Li, PhD, Professor, Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, 82 Cuiyingmen, Lanzhou 730030, Gansu Province, China. 13919951166@139.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Dong Zhou, Yu-Min Li, Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou 730030, Gansu Province, China
Peng Dong, Department of Cardiology, Aviation General Hospital, Beijing 100012, China
Fa-Cai Guo, An-Ping Zhang, Run-Ze Song, Ya-Min Zhang, Zhi-Yong Li, Dong Yuan, Chuan Yang, Department of Vascular Surgery, Lanzhou University Second Hospital, Lanzhou 730030, Gansu Province, China
Author contributions: Zhou D and Dong P contributed to the work equally and should be regarded as co-first authors; Zhou D and Li YM designed the research; Zhou D, Dong P, Guo FC and Zhang AP performed the research; Zhang YM, Li ZY, Yuan D and Yang C analyzed data; Zhou D and Dong P wrote the paper.
Supported by Gansu Provincial Natural Science Foundation, No. 1308RJZA188; and the Fundamental Research Funds for the Central Universities, No. lzujbky-2011-T03-16.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Yu-Min Li, PhD, Professor, Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, 82 Cuiyingmen, Lanzhou 730030, Gansu Province, China. 13919951166@139.com
Telephone: +86-931-8942935
Received: May 24, 2014 Peer-review started: May 24, 2014 First decision: July 15, 2014 Revised: October 20, 2014 Accepted: December 19, 2014 Article in press: December 22, 2014 Published online: February 14, 2015 Processing time: 263 Days and 6.7 Hours
Abstract
AIM: To investigate the mechanisms by which Csk-binding protein (CBP) inhibits tumor progression in esophageal carcinoma.
METHODS: A CBP overexpressing esophageal carcinoma cell line (TE-1) was established. The growth, invasion, and migration of CBP-TE-1 cells, as well as the expression of Src were then determined and compared with those in normal TE-1 cells.
RESULTS: The expression of Src was decreased by the overexpression of CBP in TE-1 cells. The growth, invasion, and migration of TE-1 cells were decreased by the overexpression of CBP.
CONCLUSION: This study indicates that CBP may decrease the metastasis of esophageal carcinoma by inhibiting the activation of Src. CBP may be a potential tumor suppressor and targeting the CBP gene may be an alternative strategy for the development of therapies for esophageal carcinoma.
Core tip: Csk-binding protein (CBP) is a ubiquitously expressed transmembrane protein and functions as a suppressor of Src-mediated tumor progression by promoting the inactivation of Src. Here, we established a CBP overexpressing esophageal carcinoma cell line (TE-1) and found that the overexpression of CBP significantly decreased the proliferation, invasion, and migration of TE-1 cells, accompanied by decreased activation of Src. These results indicate that CBP may decrease the metastasis of esophageal carcinoma by inhibiting the activation of Src. Targeting the CBP gene may be an alternative strategy for the development of therapies for esophageal carcinoma.
