Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018
MiR-206 inhibits epithelial ovarian cancer cells growth and invasion via blocking c-Met/AKT/mTOR signaling pathway.
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Dai Chunxiu, Xie Yongyong, Zhuang Xiaoping, Yuan Zhengzhong
Аннотация
BACKGROUND: MicroRNAs play important roles in the pathogenesis of various kinds of tumors. However, there are few studies on the expression profile and function of miRNAs in epithelial ovarian cancer. In this study, we performed microRNA array to compare the expression profile of microRNA in ovarian cancer tissues with noncancerous tissues.
METHODS: qRT-PCR was used to further confirm the microRNA expression levels in epithelial ovarian cancer tissues and cell lines. The function of microRNA was analyzed by overexpressing microRNA mimics followed by the analysis of cell cycle, proliferation, and metastasis. The downstream target of miR-206 was found and western blot analysis was performed to measure the activation of the downstream signaling pathway.
RESULTS: In this study, we found the expression of miR-206 was significantly down-regulated in epithelial ovarian cancer tissues and epithelial ovarian cancer cell lines. In epithelial ovarian cancer patients, downregulation of miR-206 was associated with metastasis and poor prognosis. In epithelial ovarian cancer cell lines, miR-206 contributed to the cell cycle regulation, cell apoptosis, and cancer cell metastasis. MiR-206 mimics inhibited cancer cell proliferation and metastasis, and induced cell apoptosis. Moreover, our results demonstrated that miR-206 directly targeted c-Met and repressed the activation of downstream AKT/mTOR signaling pathway.
CONCLUSION: Our results demonstrated that miR-206 was down-regulated in epithelial ovarian cancer tissues and cell lines. MiR-206 inhibits the development of epithelial ovarian cancer cell by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway.
METHODS: qRT-PCR was used to further confirm the microRNA expression levels in epithelial ovarian cancer tissues and cell lines. The function of microRNA was analyzed by overexpressing microRNA mimics followed by the analysis of cell cycle, proliferation, and metastasis. The downstream target of miR-206 was found and western blot analysis was performed to measure the activation of the downstream signaling pathway.
RESULTS: In this study, we found the expression of miR-206 was significantly down-regulated in epithelial ovarian cancer tissues and epithelial ovarian cancer cell lines. In epithelial ovarian cancer patients, downregulation of miR-206 was associated with metastasis and poor prognosis. In epithelial ovarian cancer cell lines, miR-206 contributed to the cell cycle regulation, cell apoptosis, and cancer cell metastasis. MiR-206 mimics inhibited cancer cell proliferation and metastasis, and induced cell apoptosis. Moreover, our results demonstrated that miR-206 directly targeted c-Met and repressed the activation of downstream AKT/mTOR signaling pathway.
CONCLUSION: Our results demonstrated that miR-206 was down-regulated in epithelial ovarian cancer tissues and cell lines. MiR-206 inhibits the development of epithelial ovarian cancer cell by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway.
Предметные рубрики MeSH
ApoptosisCarcinoma, Ovarian EpithelialCell CycleCell Line, TumorCell MovementCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsNeoplasm InvasivenessNeoplasms, Glandular and EpithelialOvarian NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metSignal TransductionTOR Serine-Threonine Kinases