MiR-206 inhibits epithelial ovarian cancer cells growth and invasion via blocking c-Met/AKT/mTOR signaling pathway.

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. 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. 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. 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.

Dai C ，Xie Y ，Zhuang X ，Yuan Z ... -  《-》

Down-regulated microRNA-223 or elevated ZIC1 inhibits the development of pancreatic cancer via inhibiting PI3K/Akt/mTOR signaling pathway activation.

Zhu J ，Lv J ，Chen J ，Zhang X ，Ji Y ... -  《-》

MiR-1 inhibits prostate cancer PC3 cells proliferation through the Akt/mTOR signaling pathway by binding to c-Met.

Prostate cancer (PC) is known as the most common cancer and is ranked second in cancer-related deaths in males. Accumulating evidence implicates microRNAs (miRNAs) may play key roles in tumorigenesis. We investigated the effects of microRNA-1 (miR-1) on the viability and proliferation of prostate cancer cells and the underlying mechanism. We first detected the miR-1 expression level in the PC cells by quantitative real-time PCR (qRT-PCR). The relation between the level of miR-1 and c-Met was investigated via luciferase reporter assay. Cell viability and proliferation were analyzed via MTT assay and flow cytometry in PC cells. Western blot was used for examining the related signaling pathway. MiR-1 expression was decreased and c-Met expression was increased in PC cells. Subsequently, we found that overexpression of miR-1 could inhibit viability and proliferation of PC cells functionally. Furthermore, the dual luciferase reporter assay results indicated that the c-Met is the target gene of miR-1. Western blot results indicated that this inhibition on the viability and proliferation of PC cells was via regulation of c-Met/AKT/mTOR signaling pathway. In conclusion, this study provides novel insight into the role of miR-1 in PC, and the results demonstrated that miR-1 could inhibit viability and proliferation of PC cells by targeting the c-Met/Akt/mTOR signaling pathway. MiR-1 might be a potential candidate for application in the treatment of PC.

Gao S ，Zhao Z ，Wu R ，Wu L ，Tian X ，Zhang Z ... -  《-》

MiR-99a suppressed cell proliferation and invasion by directly targeting HOXA1 through regulation of the AKT/mTOR signaling pathway and EMT in ovarian cancer.

Zhang L ，Liu XL ，Yuan Z ，Cui J ，Zhang H ... -  《-》

Comprehensive analysis of microRNA-regulated protein interaction network reveals the tumor suppressive role of microRNA-149 in human hepatocellular carcinoma via targeting AKT-mTOR pathway.

Zhang Y ，Guo X ，Xiong L ，Yu L ，Li Z ，Guo Q ，Li Z ，Li B ，Lin N ... -  《Molecular Cancer》