Oncotarget

Research Papers:

ERp29 inhibits tumorigenicity by suppressing epithelial mesenchymal transition in gastric cancer

Jing Wu, Yuanyan Yang, Shenshen Gao, Hong Jiang, Xin-Qiong Wang, Yuan Xiao, Xue-Hua Chen, Pu Li _ and Chun-Di Xu

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Oncotarget. 2017; 8:78757-78766. https://doi.org/10.18632/oncotarget.20225

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Abstract

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

Correspondence to:

Pu Li, email: leerockygood@yahoo.com

Chun-Di Xu, email: chundixu55@163.com

Keywords: ERp29, EMT, ERK1/2, AKT, gastric cancer

Received: May 04, 2017    Accepted: July 25, 2017    Published: August 12, 2017

ABSTRACT

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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