Syntaxin 6 Enhances the Progression of Epithelial Ovarian Cancer by Promoting Cancer Cell Proliferation

Document Type : Research Articles

Authors

1 Department of Obstetrics and Gynecology, The Affiliated Hospital of Youjiang Medical College for Nationalities, Baise, Guangxi 533000, P.R. China.

2 Department of Obstetrics and Gynecology, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R.China.

3 Department of General Surgery, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R.China.

Abstract

Objectives: The aim of this study is to evaluate the expression of syntaxin 6 (STX6) in epithelial ovarian cancer (EOC) and assess the effects of STX6 on the prognosis of patient. Methods: Using information from the Kaplan-Meier Plotter database, the effects of STX6 expression on overall survival (OS) and progression-free survival (PFS) in ovarian cancer patients were examined. The clinical information of 147 patients with epithelial ovarian cancer was evaluated, and immunohistochemical staining was used to identify STX6 expression in postoperative tumor specimens, and the affection of STX6 expression on patient prognosis was assessed. In addition, the expression of STX6 in tumor tissue, peritoneal metastases (PM) derived from 13 patients with epithelial ovarian cancer and 6 normal ovarian specimens was detected by PCR and Western blot. In order to investigate how STX6 affects the proliferation of tumor cells, STX6 was also over expressed and knock down in ovarian cancer cell lines. Then colony formation assay was used to explore the effect of STX6 regulating on cell proliferation. Results: Kaplan-Meier Plotter enrollment data analysis revealed that patients with overexpressed STX6 had substantially worse OS and PFS than individuals with low STX6 expression. Retrospective study revealed a significant (P<0.05) correlation between the STX6 expression and tumor classifications, tumor stage, peritoneal carcinomatosis index (PCI), and PFS survival of patients. Western blot and PCR findings for fresh samples showed that STX6 was overexpressed in both primary lesions and PM nodules of OC. SKOV3 cell proliferation was shown to be dramatically reduced by STX6 knockdown and promoted by STX6 overexpression, according to the in vitro experiments. Conclusion: STX6 may increase the progression of epithelial OC by encouraging the proliferation of cancer cells, indicating that STX6 was a viable therapeutic target of epithelial OC.

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