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자료유형
학술저널
저자정보
Man Ni (Hangzhou Bio-Science Bio-Tech Co. Ltd.) Yue Zhao (Zhejiang Chinese Medical University) Xiaoguang Wang (Hangzhou Bio-Science Bio-Tech Co. Ltd.)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.6
발행연도
2021.1
수록면
633 - 641 (9page)

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Background Although overexpression of synuclein gamma (SNCG) has been reported in several cancers, few studies have been performed onSNCG in endometrial carcinomas. Objective This study aimed to investigate the role of SNCG in the progression of endometrial carcinoma. Methods The expression pattern and function ofSNCG gene were analyzed using the Gene Expression Omnibus (GEO) and Gene Set Enrichment Analysis (GSEA) datasets. Two vector types, containing either SNCG or negative control shRNAs, were used to evaluate cell proliferation, apoptosis, and metastasis using Cell Counting Kit 8, colony formation, flow cytometry, wound-healing, transwell, and invasion assays. The relative protein levels of N-cadherin, E-cadherin, vimentin, p-PI3K, PI3K, p-AKT, AKT, p-ERK, and ERK were determined by western bloting. Results Our results revealed thatSNCG mRNA expression and SNCG protein levels in shRNA-treated SPEC2 cells were lower than in the negative control cells. Furthermore, cell proliferation, migration, and invasion were significantly inhibited in SNCG shRNA-treated cells, but apoptosis was increased. The results of western blot analysis indicated that SNCG silencing reduced the protein levels of N-cadherin, vimentin, p-PI3K, p-AKT, and p-ERK, but not those of total PI3K, AKT, and ERK. Conclusions Therefore, shRNA-mediated suppression of SNCG inhibited SPEC2 cell proliferation, migration, and invasion, and promoted SPEC2 cell apoptosis, which was presumably accomplished via regulation of the PI3K/AKT/ERK signaling pathway.

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