Survivin inhibits anti-growth effect of p53 activated by aurora B

摘要: Genomic instability and apoptosis evasion are hallmarks of cancer, but the molecular mechanisms governing these processes remain elusive. Here, we found that survivin, a member apoptosis-inhibiting gene family, aurora B kinase, chromosomal passenger protein, were co-overexpressed in various glioblastoma cell lines tumors. Notably, exogenous introduction human BJ cells was shown to decrease growth increase senescence-associated beta-galactosidase activity by activation p53 tumor suppressor. However, overexpression failed inhibit proliferation U87MG transduced with dominant-negative as well p53(-/-) mouse astrocytes. Aurora centrosome amplification Survivin induce anchorage-independent anti-proliferation drug-sensitive caused B. Overexpression both survivin further accelerated cells. Taken together, present study indicates should accelerate tumorigenesis inhibiting anti-proliferative effect suppressor is activated normal containing intact p53.