Published online Feb 14, 2015. doi: 10.3748/wjg.v21.i6.1814
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
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.
