| Summary: | 碩士 === 國立清華大學 === 生命科學系 === 90 === Mammalian cells possess a remarkable repertoire of responses to diverse stresses, particularly those inflicting genetic stability. UV, which is well known to generate photoproducts and the pyrimidine dimer may arrest cell cycle progression for DNA repair or lead to apoptosis by evoking checkpoint pathway. Previous researches in our laboratory has found that CHO.K1 cells, deficient in expression of p21 WAF1/CIP1, display UVC-induced cell death, which is promoted by the presence of anti-mitotic drugs in the cells following UVC irradiation. Here, we describe some phenomena or mechanisms to elucidate the cell death in advance. In CHO.K1 cells, UVC-induced cell death which is exacerbated in presence of colcemid (a mitotic inhibitor) belongs to apoptosis. UVC-induced DNA damage, neither ROS (Liao, 2001) nor death receptor activation, contributes to UVC-induced apoptosis. Although p21 WAF1/CIP1 is deficient in CHO.K1 cells, the cells exhibit normal nucleotide excision repair of UVC-induced DNA damage. However, the massive UVC-induced apoptosis in CHO.K1 cells is still due to the defect in p21waf1/cip1 so that CDK activity is not inhibited. During colcemid-promoted apoptosis following UVC irradiation, neither decrease of mitochondrial membrane potential nor release of Ca2+ in cytosol is observed. Over-activation of cdk1 and delay of DNA repair may result in the promoted apoptosis by colcemid.
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