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ERp19 contributes to tumorigenicity in human gastric cancer by promoting cell growth, migration and invasion

Jing Wu, Xue-hua Chen, Xin-qiong Wang, Yi Yu, Jian-min Ren, Yuan Xiao, Tong Zhou, Pu Li and Chun-di Xu _

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Oncotarget. 2015; 6:11794-11805. https://doi.org/10.18632/oncotarget.3649

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Jing Wu1,*, Xue-hua Chen2,*, Xin-qiong Wang1, Yi Yu1, Jian-min Ren1, Yuan Xiao1, Tong Zhou1, Pu Li2, Chun-di Xu1

1 Department of Pediatrics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China

2 Shanghai Key Laboratory of Gastric Neoplasms, Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China

* These authors have contributed equally to this work

Correspondence to:

Chun-di Xu, email:

Pu Li, email:

Keywords: ERp19, gastric cancer, tumorigenicity, FAK, paxillin

Received: January 07, 2015 Accepted: March 02, 2015 Published: March 26, 2015


ERp19, a mammalian thioredoxin-like protein, plays a key role in defense against endoplasmic reticulum stress. It belongs to the protein disulfide isomerize (PDI) family, whose members have been implicated in development of breast, ovarian and gastrointestinal cancers. However, the role of ERp19 in gastric cancer (GC) remains undefined. Therefore, we sought to investigate the expression and prognostic value of ERp19 in GC patients, and to explore the role of ERp19 in tumorigenicity. Expression of ERp19 in gastric tissues was assessed by immunohistochemical staining and real-time PCR in clinical samples of GC patients. Statistical analysis of clinical cases revealed that the expression levels of ERp19 were higher in tumor tissues than non-tumor tissues. And the level of ERp19 expression was correlated with tumor size, lymph node involvement and poor clinical prognosis. Furthermore, ERp19 knockdown dramatically suppressed gastric cancer cell growth, inhibited cellular migration/invasion and down-regulated the phosphorylation of FAK and paxillin, whereas ERp19 over-expression reversed these changes. We conclude that ERp19 contributes to tumorigenicity and metastasis of GC by activating the FAK signaling pathway, and may function as an oncogene in GC. ERp19 may represent a new diagnostic and prognostic marker and a novel target for the treatment of GC.

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