期刊
ONCOLOGY REPORTS
卷 27, 期 1, 页码 114-120出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2011.1451
关键词
bufalin; T24 cells; G2/M; apoptosis
类别
资金
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science, and Technology, Republic of Korea [2010-0001730]
- National Research Foundation of Korea [355-2011-1-E00113, 핵06B3503] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Bufalin, a major digoxin-like immunoreactive component of the Chinese medicine Chansu, is prepared from toad venom. This compound has been shown to exert a potential for anticancer activity against various human cancer cell lines in vitro. However, the detailed molecular mechanisms of its induction of apoptosis are still unclear. In this study, we investigated the apoptosis-inducing effect of bufalin in 124 human bladder cancer cells. Our data revealed that bufalin treatment resulted in a concentration-response growth inhibition of T24 cells by inducing cell cycle arrest at the G2/M phase and apoptosis, as evidenced by formation of apoptotic bodies, chromatin condensation and accumulation of cells in the sub-G1 phase. Apoptosis induction of T24 cells by bufalin showed correlation with proteolytic activation of caspase-3, -8 and -9, and concomitant degradation of poly (ADP-ribose) polymerases, and collapse of the mitochondria membrane potential. In addition, bufalin treatment resulted in an increase of the Bax/Bcl-2 (or Bcl-xL) ratio and caused down-regulation of inhibitor of apoptosis protein (LAP) family members. The increase in apoptosis by bufalin treatment was also associated with up-regulation of death receptor-related factors. Our data indicate that the growth inhibitory effects of bufalin occur through blockade of the G2/M phase, and that these cancer cells do not enter cell cycle progression and die through apoptosis via both intrinsic and extrinsic pathways.
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