ERp29 inhibits tumorigenicity by suppressing epithelial mesenchymal transition in gastric cancer
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Jing Wu1,2,*, Yuanyan Yang1,*, Shenshen Gao1,3,*, Hong Jiang2, Xin-Qiong Wang1, Yuan Xiao1, Xue-Hua Chen1, Pu Li1 and Chun-Di Xu1
1Department of Pediatrics, Ruijin Hospital and Ruijin Hospital North, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
2Department of Oncology, East Hospital, Tongji University School of Medicine, Shanghai, People’s Republic of China
3Department of Human Resource, Ruijin Hospital North, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
*These authors have contributed equally to this work
Pu Li, email: email@example.com
Chun-Di Xu, email: firstname.lastname@example.org
Keywords: ERp29, EMT, ERK1/2, AKT, gastric cancer
Received: May 04, 2017 Accepted: July 25, 2017 Published: August 12, 2017
ERp29 is a novel endoplasmic reticulum (ER) protein that plays an important role in protein unfolding and secretion. Recently, it has been reported to be widely implicated in control of tumorigenesis in some tumors. However, the potential function of ERp29 in gastric cancer remains poorly understood. In this study, we found that the positive rate of ERp29 in gastric cancer tissues was significantly lower than that in adjacent non-tumor tissues. And tumor with high ERp29 expression had inclinations towards smaller tumor size and earlier TNM stage. The in vitro experiments indicated that over-expression of ERp29 in gastric cancer cells significantly suppressed the proliferation and migration of tumor cells, which is consistent with the result of the in vivo animal experiments. Furthermore, our mechanistic investigations revealed that ERp29 reversed EMT process in gastric carcinoma, and its effect was related to the inactivation of ERK1/2 and AKT phosphorylation. Thus, we conclude that ERp29 acts as a tumor suppressor gene in gastric cancer, and is expected to become a novel target of the treatment of GC.
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