Abstract

Phosphatidylethanolamine-binding protein 4 (PEBP4) has previously been reported to be upregulated in various cancers. However, the physiological functions of PEBP4 in gastric cancer are still unknown. Aiming to clarify the properties and role of PEBP4 in the development and invasion of gastric cancer, we performed several biological assays and a knockdown assay. The expression level of PEBP4 was shown to be significantly upregulated in gastric cancer tissue samples, and knockdown of the expression of PEBP4 induced significant inhibitory effects on cell proliferation, migration and invasiveness. In addition, it was demonstrated that PEBP4 was associated with the development and invasion of gastric cancer cells through activation of the PI3K/Akt signaling pathway. Our findings supported the hypothesis that PEBP4 might be a novel potential drug target for the treatment of gastric cancer.

Highlights

  • Gastric cancer is one of the main contributors to cancer-related mortality worldwide [1]

  • Our results show that the effects of Phosphatidylethanolamine-binding protein 4 (PEBP4) on the tumorigenesis and metastasis of gastric cancer depend on the dysregulation of the PI3K/Akt signaling pathway

  • PEBP4 has been reported to be upregulated in pancreatic ductal adenocarcinoma (PDAC), and knockdown of PEBP4 has been shown to result in the attenuation of cancer cell growth, migration, and metastasis of PDAC cancer cells [10]

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Summary

Introduction

Gastric cancer is one of the main contributors to cancer-related mortality worldwide [1]. Despite recent developments in early diagnosis and other novel therapeutic strategies, the median survival time for advanced gastric cancer patients has still remained at approximately 7 months [2, 3]. Investigations into the molecular mechanisms of invasion and metastasis of gastric cancer seek to contribute to the development of a novel and effective drug target. The upregulation of PEBP4 was reported to be associated with the proliferation, invasion and drug resistance of tumor cells [9, 10]. We silenced the expression of PEBP4 by specific siRNA in gastric cancer cell lines and investigated the effects of PEBP4 on cell proliferation, migration and invasion. Our results show that the effects of PEBP4 on the tumorigenesis and metastasis of gastric cancer depend on the dysregulation of the PI3K/Akt signaling pathway

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