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MicroRNAs (miRNAs) have been implicated in the maintenance of the cancerstem cell (CSC) phenotype via their ability to affect expression of genes andproteins that regulate cell proliferation and/or cell death. Thus, identificationof CSC-related miRNAs would provide information for a better understanding ofCSCs. Here, we compared the miRNA profiles of CD133+ and CD133- primary hepatocellularcarcinoma (HCC) subpopulations and found upregulation of 5 miRNAs in CD133- subpopulations,including hsa-miR-150, which may be involved in maintenance of the CD133+ liverCSC phenotype. We also show that miR-150 interacts with the 3'UTR of c-Myb mRNAand overexpression of miR-150 downregulates c-Myb protein levels. Furthermore,overexpression of miR-150 lead to a significant reduction of CD133+ cells, accompaniedby significant inhibition of cell growth and tumorsphere formation. In addition,overexpression of miR-150 induces cell cycle arrest and apoptosis in CD133+ cells.Consistent with the outcome of cell cycle arrest and cell apoptosis, Western blottingresults demonstrate that the cell cycle regulator cyclin D1 and cell survivalregulator Bcl-2 are decreased in cells transfected with miR-150. Collectively,our findings demonstrate for the first time that miR-150 may be involved in liverCSC self-renewal, potentially via modulation of the downstream target c-Myb.

microRNA-150 inhibits human CD133-positive liver cancer stem cells through negative regulation of the transcription factor c-Myb