Pan Changqing, Wang Dan, Zhang Yao, Yu Wenliang
Department of Obstetrics and Gynecology, Mianyang Central Hospital, Mianyang, Sichuan, P.R. China.
Oncol Res. 2016 Oct 27;24(6):429-435. doi: 10.3727/096504016X14685034103518.
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.
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。
