PMID- 31411791 OWN - NLM STAT- MEDLINE DCOM- 20200331 LR - 20211204 IS - 1447-0756 (Electronic) IS - 1341-8076 (Linking) VI - 45 IP - 11 DP - 2019 Nov TI - Effects of microRNA-1271 on ovarian cancer via inhibition of epithelial-mesenchymal transition and cisplatin resistance. PG - 2243-2254 LID - 10.1111/jog.14079 [doi] AB - AIM: Efficacy of platinum based-chemotherapy is limited by cisplatin (DDP) resistance, however, the underlying mechanism of cisplatin resistance remains unclear. We aimed to investigate the role of miR-1271 in cisplatin-resistant ovarian cancer cells. METHODS: Transfection of miR-1271 mimic and inhibitor was performed to study the role of miR-1271 in ovarian cancer. Cell viability was assessed by Cell Counting Kit (CCK)-8 assay. Flow cytometry was used to determine the apoptosis rates. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot were used to detect mRNA and protein expressions. Target predicted by Targetscan7.2 was confirmed by dual-luciferase activity assay. Mammalian target of rapamycin (mTOR) siRNA (simTOR) co-transfection was performed to verify the role of mTOR in the suppression effect of miR-1271 on ovarian cancer. RESULTS: In SKOV3 cells, miR-1271 overexpression significantly decreased cell viability and up-regulated apoptosis rate (from 5.54% of control to 24.03%). MiR-1271 adversely affected SKOV3 cell migration and invasion, and induced the upregulation of E-cadherin and downregulation of N-cadherin and alpha-smooth muscle actin (alpha-SMA). Moreover, SKOV3/DDP cells had a lower miR-1271 level, and enhancing miR-1271 contributed strongly to cisplatin-induced apoptosis through altering the expressions of B-cell lymphoma-2 associated X protein (BAX), cleaved caspase-3 and B-cell lymphoma 2 (Bcl-2). In contrast, the opposite result was observed in miR-1271 inhibitor. mTOR was identified to be a target of miR-1271. SimTOR partially reversed the increased cell viability under the effect of miR-1271 inhibitor. CONCLUSION: Our data indicate that miR-1271 can inhibit the ovarian cancer epithelial-mesenchymal transition (EMT) and sensitize resistant cells to cisplatin-induced apoptosis through blocking mTOR expression. CI - (c) 2019 Japan Society of Obstetrics and Gynecology. FAU - Chen, Yanyan AU - Chen Y AD - Department of Outpatient Pharmacy, Ningbo Women & Children's Hospital, Ningbo, China. FAU - Wang, Li AU - Wang L AD - Department of Outpatient Pharmacy, Ningbo Women & Children's Hospital, Ningbo, China. FAU - Zhou, Jiefang AU - Zhou J AD - Department of Clinical Pharmacology, Shaoxing Traditional Chinese Medicine Hospital, Shaoxing, China. LA - eng PT - Journal Article DEP - 20190814 PL - Australia TA - J Obstet Gynaecol Res JT - The journal of obstetrics and gynaecology research JID - 9612761 RN - 0 (Antineoplastic Agents) RN - 0 (MIRN1271 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (RNA, Small Interfering) RN - EC 2.7.1.1 (MTOR protein, human) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) RN - Q20Q21Q62J (Cisplatin) SB - IM MH - Antineoplastic Agents/*pharmacology MH - Apoptosis/drug effects MH - Cell Line, Tumor MH - Cell Survival/drug effects MH - Cisplatin/*pharmacology MH - Down-Regulation MH - Drug Resistance, Neoplasm MH - Epithelial-Mesenchymal Transition/*genetics MH - Female MH - Humans MH - MicroRNAs/*metabolism MH - Ovarian Neoplasms/drug therapy/*genetics MH - RNA, Small Interfering/drug effects MH - TOR Serine-Threonine Kinases/metabolism MH - Up-Regulation OTO - NOTNLM OT - E-cadherin OT - apoptosis OT - dual-luciferase activity assay OT - mammalian target of rapamycin OT - microRNA-1271 EDAT- 2019/08/15 06:00 MHDA- 2020/04/01 06:00 CRDT- 2019/08/15 06:00 PHST- 2018/12/18 00:00 [received] PHST- 2019/07/15 00:00 [accepted] PHST- 2019/08/15 06:00 [pubmed] PHST- 2020/04/01 06:00 [medline] PHST- 2019/08/15 06:00 [entrez] AID - 10.1111/jog.14079 [doi] PST - ppublish SO - J Obstet Gynaecol Res. 2019 Nov;45(11):2243-2254. doi: 10.1111/jog.14079. Epub 2019 Aug 14.