Caspase-3 Promotes Genetic Instability and Carcinogenesis

摘要: Apoptosis is typically considered an anti-oncogenic process since caspase activation can promote the elimination of genetically unstable or damaged cells. We report that a central effector apoptosis, caspase-3, facilitates rather than suppresses chemical- and radiation-induced genetic instability carcinogenesis. found significant fraction mammalian cells treated with ionizing radiation survive despite caspase-3 activation. Moreover, this sublethal promoted persistent DNA damage oncogenic transformation. In addition, chemically induced skin carcinogenesis was significantly reduced in mice deficient caspase-3. Furthermore, attenuation of EndoG activity transformation, identifying EndoG as downstream pathway. Our findings suggest acting broad inhibitor carcinogenesis, may contribute to genome play pivotal role tumor formation following damage.