MicroRNA 1301 inhibits cisplatin resistance in human ovarian cancer cells by regulating EMT and autophagy

被引:2
|
作者
Yu, J-L [1 ]
Gao, X. [1 ]
机构
[1] Chifeng City Hosp, Dept Gynecol, Chifeng City, Inner Mongolia, Peoples R China
关键词
Ovarian cancer; Drug resistance; Cisplatin; MicroRNA1301; NF-kappa B; Autophagy; Proliferation; EMT;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: Ovarian cancer is prone to chemoresistance. leading to poor out-comes in patients. MicroRNA 1301 plays a regulatory role in multiple tumors. However, whether microRNA 1301 regulates cisplatin resistance in ovarian cancer cells remains unclear. MATERIALS AND METHODS: The ovarian cancer SKOV3 cell line and the human ovarian cancer cisplatin-resistant strain cell SKOV3/ DDP were cultured in vitro and microRNA1301 expression was analyzed by Real time PCR. MicroRNA1301 mimics and microRNA 1301 were transfected into SKOV3/DDP. respectively fol-lowed by analysis of cell proliferation by MTT assay, cell invasion, expression of autophagy genes ATG5 and Beclin1 and EMT-related transcription factors Snail and Slug by Real time PCR, expression of NF-kappa B and E-cadherin and N-cadherin by Western blot. RESULTS: MicroRNA 1301 expression was significantly increased in SKOV3/DDP cells compared with that in SKOV3 cells (p<0.05). MicroR-NA1301 mimics transfection into SKOV3/DDP up-regulated microRNA1301 expression, promoted cell proliferation, and invasion, inhibit-ed ATG5 and Beclinl expression, and promoted Snail and Slug expression, decreased E-cadherin expression and increased N-cadherin and NF-kappa B expression, compared with the control group, the differences were statistically significant (p<0.05). MicroRNA1301 inhibitor transfection into SKOV3/DDP cells could down-regulate the expression of microRNA1301 and significantly reversed the above changes. Compared with the control group, differences were statistically significant (p<0.05). CONCLUSIONS: Targeting microRNA1301 can inhibit the proliferation of cisplatin-resistant cells and the development of EMT in human ovarian cancer cells by inhibiting the NF-kappa B signaling pathway, thereby inhibiting the occurrence and development of drug-resistant ovarian cancer.
引用
收藏
页码:1688 / 1696
页数:9
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