Silencing Bmi1 inhibits the proliferation and invasiveness in CD133+ cancer stem cells of Hep-2 cells

It has been shown that over-expression of B-cell-specific Moloney murine leukemia virus insertion site 1 (Bmi1) play a key role in maintaining the stem-like properties in CD133+ Hep-2 cells. This study was aimed at investigating the effects of silencing Bmi11 on CD133+ Hep-2 cells. Bmi1 silencing was achieved by transfection with the vectors expressing small hairpin RNA (shRNA) versus Bmi1. Cell proliferation was detected in a micro plate reader with Cell Counting Kit-8, cell apoptosis was analyzed by flow cytometry and Cell invasion were detected by trans-well invasion assays. The study found that silencing Bmi1 inhibited the proliferation of Hep-2 CD133+ cells, and that the proportion of apoptotic cells were enhanced and invasion were inhibited by knockdown of Bmi1 in CD133+ Hep-2 cells. Furthermore, mRNA and protein of P16 were increased strikingly after Bmi1 silencing. The over-expression of Bmi1 is responsible for stem-like properties in CD133+ Hep-2 cells, indicating that silencing Bmi1 expression in the cells might be developed as an efficient therapy.