Baf155 Inhibits Proliferation And Migration By Up-Regulation Of P16 And Inactivation Of Pi3k/Akt And Wnt/Beta-Catenin Pathways In Pc3 Cells

Recent studies have established that BAF155 possess tumor-suppressor activity in human colorectal cancer SNUC2B and human ovarian carcinoma SKOV3 cells. However, the function of BAF155 in human prostate cancer PC3 cells has not been well analyzed. Therefore, the aim of our study was to examine the status of BAF155 in PC3 cells, and explore the mechanism of BAF155 expression loss in PC3. Cell proliferation (MTT) assay, apoptosis assay and migration assay were respectively used to explore the viability, apoptosis and migration of PC3 cells. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to confirm the mRNA expression level of BAF155. Western blot analysis was performed to determine the protein expression levels of BAF155, p16, and key kinases involved in PI3K/AKT and Wnt/beta-catenin pathways. We identified the BAF155 was completely lost in PC3 cells compared with normal cells. Compared with control, over-expression of exogenous BAF155 could inhibit proliferation and migration while promoting apoptosis of PC3 cells (P < 0.05), which could be restored to the normal level by silencing of exogenous BAF155. The further studies on protein expression implied that overexpression of BAF155 markedly up-regulated the expression of p16 while down-regulating the expressions of key kinases involved in PI3K/AKT and Wnt/beta-catenin pathways when compared with that in control (P < 0.05). The effects of BAF155 over-expression on proteins could be reversed by silencing of exogenous of BAF155. In conclusion, over-expression of BAF155 could inhibit proliferation and migration while inducing apoptosis of PC3 cells through up-regulating p16 and inactivating PI3K/Akt and Wnt/beta-catenin pathways.