Abstract
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.
Highlights
Gastric cancer (GC) is the fourth most common malignancy and the second leading cause of cancer related death worldwide
We found that ERp19 was expressed in the cytoplasm of gastric carcinoma cells (Fig. 1B)
These findings indicate that ERp19 was overexpressed in gastric cancer tissues and most GC cell lines whether ERp19 expression was correlated with clinicopathological features remained to be determined
Summary
Gastric cancer (GC) is the fourth most common malignancy and the second leading cause of cancer related death worldwide. Half of all GC cases occur in Eastern Asia [1,2,3], where most patients are diagnosed at an advanced stage of GC [4]. Despite the increasing efficacy of surgical treatments and adjuvant therapy, nearly 60% of those patients affected succumb to GC [5]. GC is a heterogeneous disease, and prognosis is difficult to predict from histological analysis. Tumor progression is thought to be controlled by multiple factors at multiple stages involving the activation of oncogenes or inactivation of tumor suppressor genes. Promising molecules being useful for GC early diagnosis and targeted therapy are still limited. Elucidating the molecular mechanisms responsible for GC carcinogenesis has the potential to highlight valuable prognostic markers and targets for treatment of this disease
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