The tumor suppressor p33ING1b enhances taxol-induced apoptosis by p53-dependent pathway in human osteosarcoma U2OS cells

p33(ING1b) can stimulate cell cycle arrest, DNA repair, apoptosis and chemosensitivity. The actions of p33(ING1b) involve p53-dependent and p53-independent mechanisms. To investigate if the p33(ING1b) isoform is involved in the chemosensitivity of osteosarcoma cells, p33(ING1b) was overexpressed in p53+/+ U2OS cells or p53-mutant MG63 cells, and then cell growth arrest and apoptosis were assessed after treatment with taxol. The results showed that p33(ING1b) markedly increased taxol-induced growth inhibition and apoptosis in p53+/+ U2OS cells, but not in p53-mutant MG63 cells. Moreover, ectopic expression of p33(ING1b) could obviously upregulate p53, p21(WAF1) and box protein levels and activate caspase-3 in taxol-freated U2OS cells. Taken together, our data demonstrate that p33(ING1b) enhances taxol-induced apoptosis through p53-dependent pathway in human osteosarcoma cells. p33(ING1b) may be an important marker and/or therapeutic target in the prevention and treatment of osteosarcoma.