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Korean Journal of Urology 2012-Nov

Induction of apoptosis of bladder cancer cells by zinc-citrate compound.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
Kiungo kimehifadhiwa kwenye clipboard
Sung-Hoo Hong
Yong Sun Choi
Hyuk Jin Cho
Ji Youl Lee
Tae-Kon Hwang
Sae Woong Kim

Maneno muhimu

Kikemikali

OBJECTIVE

Zinc is one of the trace minerals in the body and is known to have an anticancer effect by inducing apoptosis in prostate cancer. We aimed to investigate the antiproliferative effects of a zinc-citrate compound in bladder cancer.

METHODS

A bladder cancer cell line (MBT-2) was treated with a zinc-citrate compound at different time intervals and concentrations. Mitochondrial (m)-aconitase activity was determined by use of the aconitase assay. DNA laddering analysis was performed to investigate apoptosis of MBT-2 cells. The molecular mechanism of apoptosis was investigated by Western blot analysis of p53, p21(waf1), Bcl-2, Bcl-xL, and Bax and also by caspase-3 activity analysis.

RESULTS

Treatment with the zinc-citrate compound resulted in a time- and dose-dependent decrease in cell number of MBT-2 cells. M-aconitase activity was significantly decreased. DNA laddering analysis indicated apoptosis of MBT-2 cells. The zinc-citrate compound increased the expression of p21(waf1) and p53 and reduced the expression of Bcl-2 and Bcl-xL proteins but induced expression of Bax protein. The zinc-citrate compound induced apoptosis of MBT-2 cells by activation of the caspase-3 pathway.

CONCLUSIONS

We have shown that a zinc-citrate compound induces apoptotic cell death in a bladder cancer cell line, MBT-2, by caspase-3 activation through up-regulation of apoptotic proteins and down-regulation of antiapoptotic proteins.

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