期刊
CANCER RESEARCH
卷 68, 期 15, 页码 6468-6476出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-08-0896
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资金
- NCI NIH HHS [P01 CA077839, P01 CA077839-05, P01-CA-77839] Funding Source: Medline
- NICHD NIH HHS [R37-HD12304, R37 HD012304] Funding Source: Medline
- NIDA NIH HHS [R37 DA006668, R37-DA06668] Funding Source: Medline
- NIDDK NIH HHS [R01 DK062112, R37-DK-47297, P30-DK-58404, R01 DK062112-07, R01-DK-62112, R37 DK047297-15, R37 DK047297, P30 DK058404] Funding Source: Medline
Although endocannabinoid signaling is important for certain aspects of gastrointestinal homeostasis, the role of the cannabinoid receptors (CB) in colorectal cancer has not been defined. Here we show that CB1 expression was silenced in human colorectal cancer due to methylation of the CB1 promoter. Our genetic and pharmacologic studies reveal that loss or inhibition of CB1 accelerated intestinal adenoma growth in Apc(Min/+) mice whereas activation of CB1 attenuated intestinal tumor growth by inducing cell death via down-regulation of the antiapoptotic factor survivin. This down-regulation of survivin by CB1 is mediated by a cyclic AMP-dependent protein kinase A signaling pathway. These results indicate that the endogenous cannabinoid system may represent a potential therapeutic target for prevention or treatment of colorectal cancer.
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