JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Overexpression of microRna-200c in CD44+CD133+ CSCS inhibits the cellular migratory and invasion as well as tumorigenicity in mice.

Cancer stem cells (CSCs) are believed to be responsible for drug resistance, metastasis of tumors. To investigate the biological characteristics of CD44+CD133+CSCs with over- expressing microRNA-200c (miR-200c), and to provide evidences for miR-200c as a tumor suppressor to treat melanoma. CD44+CD133+CSCs were isolated from the mouse melanoma B16F10 cell line by using immune magnetic activated cell sorting. The lentivirus miR-200c was transduced into the cells, and the effect of miR-200c overexpression on the biological characteristics of B16F10 CD44+ CD133+CSCs was analyzed by a series assays. The stable overexpression of miR-200c in B16F10 CD44+CD133+CSCs obviously resulted in downregulation of zinc-finger E-box binding homeobox 1 expression, reduction of the cell proliferation, colony forming, cell migratory and invasion ability in vitro as well as tumorigenicity in vivo compared with those of the B16F10 cells and B16F10 non-CD44+ CD133+CSCs. These findings suggest that the miR-200c overexpression as a novel strategy to target therapy of melanoma CSCs.

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