期刊
MOLECULAR BIOLOGY REPORTS
卷 40, 期 11, 页码 6287-6293出版社
SPRINGER
DOI: 10.1007/s11033-013-2741-x
关键词
WIN55,212-2; BEL-7402 cells; Cannabinoid receptor; PPAR gamma; c-myc; Apoptosis
资金
- National Science Foundation of China [81141101]
- Scientific and Technological Project of Guangzhou City [2009J1-C361]
Cannabis sativa has long been used as a traditional medicine in China. Among its effective compounds are cannabinoids. This study determined the effect of WIN55,212-2 (WIN), a synthetic cannabinoid, on the BEL-7402 human hepatocellular carcinoma (HCC) cell line. The results showed that WIN could decrease the proliferation of BEL-7402 cells. Moreover, WIN could cause apoptosis of the cells via up-regulation of Bax expression, down-regulation of Bcl-2 expression, induction of the mitochondrial membrane potential, increase of caspase-3, -8 and -9 activities, and induction of the cleavage of caspase-3 and poly-ADP-ribose polymerase (PARP). The WIN-induced apoptosis was accompanied by the up-regulation of PPAR gamma expression, the activation of PPAR gamma DNA binding activity, and a down-regulation of PPAR gamma target oncogene c-myc. Conversely, the effects of WIN could be attenuated by PPAR gamma antagonist GW9662, and the WIN induced PPAR gamma expression was partially attenuated by AM630, a cannabinoid receptor-2 antagonist, whereas the WIN-induced reduction of c-myc expression was partially restored by GW9662. Collectively, our results suggest that WIN can decrease the proliferation and cause apoptosis of the BEL-7402 cells via a mitochondrial-caspase pathway and mediated by PPAR gamma. These results may provide a basis for the application of WIN in HCC treatment.
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