miR-495 promotes apoptosis and inhibits proliferation in endometrial cells via targeting PIK3R1

被引:18
|
作者
Tan, Aili [1 ]
Luo, Ruoyu [1 ]
Ruan, Peng [2 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Obstet & Gynecol, Wuhan 430060, Hubei, Peoples R China
[2] Wuhan Univ, Renmin Hosp, Dept Oncol, 238 Jiefang Rd, Wuhan 430060, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Endometrial cancer; miR-495; PIK3R1; VEGF; Apoptosis; Proliferation; CANCER; EXPRESSION; GROWTH; ANGIOGENESIS; MANAGEMENT; TUMOR;
D O I
10.1016/j.prp.2019.01.020
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Endometrial cancer (EC) is a huge threat to women's health. The aims of this study were to investigate the role of microRNA (miR)-495 in the proliferation and apoptosis of EC cells in vitro. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect the mRNA levels. In addition, dual-luciferase reporter assay was used to verified that PIK3R1 was a target of miR-495. After transfection with miR-495 mimics, Cell Counting Kit 8 (CCK-8) assay was performed to evaluate the cell viability of EC cells. The protein expression of PIK3R1, vascular endothelial growth factor (VEGF), Bcl-2, Bax, caspase 3 after transfection was analyzed using western blotting. Furthermore, cell apoptosis rate of EC cells was evaluated by flow cytometry. These results showed that miR-495 was significantly down-regulated in tumor tissues compared with the adjacent normal tissues, while PIK3R1 was up-regulated. The proliferation of the EC cells that were transfected with miR-495 mimics was markedly inhibited, and apoptosis was significantly promoted. In addition, down-regulated expression of PIK3R1, Bcl-2, VEGF expression and upregulated expression of Bax and caspase 3 expression were observed after transfected with miR-495 mimic. Together these findings indicated that miR-495 acts as a tumor suppressor gene by directly targeting PIK3R1 at the post-transcriptional level in EC cells in vitro.
引用
收藏
页码:594 / 599
页数:6
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