Objective To explore the apoptosis inducing effects of arsenic trioxide (As
2O3) on human bladder cancer cells and elucidate possible mechanisms.
Methods After treatment with As2O3, the growth inhibition rates of human bl
adder cancer cell line BIU-87 were studied by MTT and cell counts methods.
DNA synthesis rates were detected by H-3-TdR assay. The morphological chang
es of cancer cells were observed by light and electronic microscopy and cel
l apoptosis rates were detected by TdT-mediated dUTP nick end labeling (TUN
EL). bcl-2 gene expression of BIU-87 cells was observed by strept avidin-bi
otin complex (SABC) immunohistochemical method.
Results As2O3 could effectively inhibit the growth of BIU-87 (P < 0.05), wh
ich were time and concentration dependent. The inhibition rate of 4.0 <mu>m
ol/l As2O3 for DNA synthesis of cancer cells was 55.64% (P<0.01). Partial c
ancer 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(2)O(3) can significantly induce apoptosis in bladder cancer c
ells 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.