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Background  Cancer stem cells (CSCs) are believed to be ‘seed cell’ in cancer recurrence and metastasis. MicroRNAs (miRNAs) can play an important role in the progression of primary tumor towards metastasis by regulating the epithelial-mesenchymal transition (EMT). The goal of this study was to investigate the effect of miRNA-200c overexpression on the EMT, tumorigenicity and metastasis of epithelial ovarian cancer (EOC) CSCs.    Methods  The EOC CD117 + CD44 + CSCs were isolated from the human ovarian cancer cell line SKOV3 by using a magnetic-activated cell sorting system, and the lentivirus miR-200c transduced CSCs were then selected for the study. The assays of colony forming, wound healing, cellular migration  in vitro  and tumor progression  in vivo  were performed.    Results  The miR-200c expression was reduced in the CD117 + CD44 + CSCs compared with the non-CD117 + CD44 + CSCs. However, the stable overexpression of the miR-200c in the CD117 + CD44 + CSCs resulted in a significant down-regulation of ZEB-1 and the Vimentin expression, an upregulation of the E-cadherin expression as well as a decrease of colony forming, migratory and invasion  in vitro . Importantly, the miR-200c overexpression significantly inhibited the CD117 + CD44 + CSCs xenograft growth and lung metastasis  in vivo  in nude mice by inhibition of the EMT. In addition, the down-regulation of ZEB-1 showed the same efficacy as the miR-200c overexpression in the CD117 + CD44 + CSCs.    Conclusion  These findings from this study suggest that the miR-200c overexpression may be considered a critical approach for the EOC CD117 + CD44 + CSCs in clinical trials.

journal of ovarian research

MicroRNA-200c overexpression inhibits tumorigenicity and metastasis of CD117+CD44+ ovarian cancer stem cells by regulating epithelial-mesenchymal transition