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微小RNA-1284抑制卵巢癌细胞系OVCAR3的细胞活力并诱导其凋亡。

MicroRNA-1284 Inhibits Cell Viability and Induces Apoptosis of Ovarian Cancer Cell Line OVCAR3.

作者信息

Pan Changqing, Wang Dan, Zhang Yao, Yu Wenliang

机构信息

Department of Obstetrics and Gynecology, Mianyang Central Hospital, Mianyang, Sichuan, P.R. China.

出版信息

Oncol Res. 2016 Oct 27;24(6):429-435. doi: 10.3727/096504016X14685034103518.

Abstract

Ovarian cancer is a malignancy with high mortality among women. Multiple reports show that microRNAs (miRs) act as regulators in ovarian cancer inhibition, while the role of miR-1284 in ovarian cancer is still unknown. This study aimed to investigate the effects of miR-1284 on ovarian cancer cells. Human ovarian cancer cell line OVCAR3 was cultured and transfected with miR-1284 mimics, inhibitors, or control. Viability and apoptosis of transfected cells were then determined by MTT assay, BrdU assay, and flow cytometry. Expression changes of p27, p21, and PI3K/Akt pathway-related proteins were measured by Western blot. Results showed that miR-1284 overexpression suppressed cell viability while increasing the apoptosis in OVCAR3 cells. Moreover, the expression level of p27 was upregulated by miR-1284 overexpression. Furthermore, miR-1284 overexpression and Akt inhibitor GSK690693 downregulated the levels of p-Akt and Bcl-2 while upregulating the levels of Bax and caspase 3. However, miR-1284 suppression attenuated the regulatory effects of GSK690693 on these proteins. In conclusion, miR-1284 could inhibit cell viability via regulating the expression of p27 and induce apoptosis via regulating the PI3K/Akt pathway in OVCAR3 cells.

摘要

卵巢癌是女性中死亡率较高的恶性肿瘤。多项报告显示,微小RNA(miR)在卵巢癌抑制中起调节作用,而miR-1284在卵巢癌中的作用尚不清楚。本研究旨在探讨miR-1284对卵巢癌细胞的影响。培养人卵巢癌细胞系OVCAR3,并分别用miR-1284模拟物、抑制剂或对照进行转染。然后通过MTT法、BrdU法和流式细胞术测定转染细胞的活力和凋亡情况。通过蛋白质印迹法检测p27、p21和PI3K/Akt通路相关蛋白的表达变化。结果显示,miR-1284过表达抑制了OVCAR3细胞的活力,同时增加了细胞凋亡。此外,miR-1284过表达上调了p27的表达水平。此外,miR-1284过表达和Akt抑制剂GSK690693下调了p-Akt和Bcl-2的水平,同时上调了Bax和caspase 3的水平。然而,miR-1284抑制减弱了GSK690693对这些蛋白的调节作用。总之,miR-1284可通过调节p27的表达抑制OVCAR3细胞的活力,并通过调节PI3K/Akt通路诱导细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ede5/7838609/7ede69538785/OR-24-429-g001.jpg

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