RESUMO
MicroRNA (miR)29b is a key tumor regulator. It can inhibit tumor cell proliferation, induce apoptosis, suppress tumor invasion and migration, thus delaying tumor progression. Our previous studies revealed an increased level of miR29b in hepatoma 22 (H22) cells in ascites tumorbearing mice. The present study investigated the effect of miR29b on proliferation and apoptosis of hepatocellular carcinoma ascites H22 cells and its association with the transforming growth factorß1 (TGFß1) signaling pathway and p53mediated apoptotic pathway. Briefly, H22 cells were transfected with miR29b3p (hereinafter referred to as miR29b) mimic or miR29b inhibitor. MTS cell proliferation assay and flow cytometry were used to analyze cell viability and apoptosis. The expression change of the TGFß1 signaling pathway and p53mediated apoptotic pathway were detected by reverse transcriptionquantitative PCR, western blotting and immunofluorescence. Furthermore, cells were treated with exogenous TGFß1 and TGFß1 small interfering RNA to evaluate the crosstalk between TGFß1 and p53 under miR29b regulation. The overexpression of miR29b decreased cell viability, increased cell apoptosis, activated the TGFß1 signaling pathway and p53mediated apoptotic pathway. Conversely, these effects were reversed by the miR29b inhibitor. Moreover, the effect of miR29b mimic was further increased after treating cells with exogenous TGFß1. The activation of the TGFß1 signaling pathway and p53mediated apoptotic pathway induced by miR29b overexpression were reversed by TGFß1 inhibition. In summary, these data indicated that miR29b has an important role in proliferation and apoptosis of H22 cells by regulating the TGFß1 signaling pathway, the p53dependent apoptotic pathway, and the crosstalk between TGFß1 and p53.