Upregulation of SCNN1A Promotes Cell Proliferation, Migration, and Predicts Poor Prognosis in Ovarian Cancer Through Regulating Epithelial–Mesenchymal Transformation

波形蛋白 卵巢癌 癌症研究 生物 癌症 基因敲除 细胞生长 上皮-间质转换 基因沉默 异位表达 污渍 肿瘤科 癌基因 细胞周期 细胞培养 转移 医学 免疫组织化学 免疫学 遗传学 基因
作者
Lan Wu,Zhonghui Ling,Huan Wang,Xinyan Wang,Jing Gui
出处
期刊:Cancer Biotherapy and Radiopharmaceuticals [Mary Ann Liebert]
卷期号:34 (10): 642-649 被引量:22
标识
DOI:10.1089/cbr.2019.2824
摘要

Background: There is little knowledge about the biological roles and clinical significance of SCNN1A in ovarian cancer. Thus, the objective of this study was to investigate the biological functions and prognosis value of SCNN1A in ovarian cancer to further seek a potential therapeutic target for patients with ovarian cancer. Materials and Methods: First, the expression level of SCNN1A in ovarian cancer samples obtained from ONCOMINE database was determined, and its expression in cell lines was also investigated. Moreover, correlation analysis was performed to determine the relationship between SCNN1A expression and prognosis in ovarian cancer patients according to the data obtained from GEPIA database and Kaplan–Meier plotter website. The biological roles of SCNN1A on cell growth, migration, and invasion were then examined by knockdown of SCNN1A in ovarian cancer cell line SK-OV-3. Ultimately, Western blotting analysis was carried out to investigate the expression of epithelial–mesenchymal transformation markers (including E-cadherin, N-cadherin, Vimentin, and Snail) after silencing SCNN1A. Results: Based on the ONCOMINE-related data and cell lines, SCNN1A was observed to be overexpressed in ovarian cancer samples and cell lines. Survival analysis showed that high expression of SCNN1A was associated with poor overall survival and progression-free survival in ovarian cancer patients. In addition, SCNN1A silence remarkably blocked SK-OV-3 cell growth ability, migration, and invasion potential. Western blotting results showed that SCNN1A silence led to an increase in E-cadherin, whereas a decrease in N-cadherin, Vimentin, and Snail in SK-OV-3 cells. Increased E-cadherin and decreased N-cadherin, Vimentin, as well as Snail inhibited cell invasion of ovarian cancer. Conclusions:SCNN1A might exert crucial roles in cell growth and invasion and migration in ovarian cancer, and might be a potential indicator for prognosis and a therapeutic target for ovarian cancer patients.
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