Objective To explore the apoptosis inducing effects of arsenic trioxide (As 2O 3) on human bladder cancer cells and elucidate possible mechanisms Methods After treatment with As 2O 3, the growth inhibition rate...
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Objective To explore the apoptosis inducing effects of arsenic trioxide (As 2O 3) on human bladder cancer cells and elucidate possible mechanisms Methods After treatment with As 2O 3, the growth inhibition rates of human bladder cancer cell line BIU 87 were studied by MTT and cell counts methods DNA synthesis rates were detected by 3H TdR assay The morphological changes of cancer cells were observed by light and electronic microscopy and cell apoptosis rates were detected by TdT mediated dUTP nick end labeling (TUNEL) bcl 2 gene expression of BIU 87 cells was observed by strept avidin biotin complex (SABC) immunohistochemical method Results As 2O 3 could effectively inhibit the growth of BIU 87 ( P <0 05), which were time and concentration dependent The inhibition rate of 4 0?μmol/L As 2O 3 for DNA synthesis of cancer cells was 55 64% ( P <0 01) Partial cancer cells presented the characteristic morphological changes of apoptosis which depended on the time of exposure to drug ( P <0 05) bcl 2 expression of BIU 87 cells was decreased significantly ( P <0 05) Conclusion As 2O 3 can significantly induce apoptosis in bladder cancer cells by down regulating the expression of the bcl 2 gene and inhibiting DNA synthesis This provides a potentially effective method for prevention and cure of human bladder cancer
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