AI Article Synopsis
- The endocannabinoid system, specifically CB2, plays a complex role in colon cancer, with evidence suggesting it may influence immune responses.
- In experiments with mice, those lacking CB2 exhibited a higher occurrence of precancerous lesions and increased tumor development, alongside changes in immune cell populations.
- Analysis of human genomic data indicates a link between specific variants and colon cancer incidence, highlighting the potential for CB2 as a target for cancer prognosis and treatment.
Article Abstract
The endocannabinoid system, particularly cannabinoid receptor 2 (CB2 in mice and CNR2 in humans), has controversial pathophysiological implications in colon cancer. Here, we investigate the role of CB2 in potentiating the immune response in colon cancer in mice and determine the influence of variants in humans. Comparing wild-type (WT) mice to CB2 knockout (CB2) mice, we performed a spontaneous cancer study in aging mice and subsequently used the AOM/DSS model of colitis-associated colorectal cancer and a model for hereditary colon cancer (Apc). Additionally, we analyzed genomic data in a large human population to determine the relationship between variants and colon cancer incidence. Aging CB2 mice exhibited a higher incidence of spontaneous precancerous lesions in the colon compared to WT controls. The AOM/DSS-treated CB2 and ApcCB2 mice experienced aggravated tumorigenesis and enhanced splenic populations of immunosuppressive myeloid-derived suppressor cells along with abated anti-tumor CD8+ T cells. Importantly, corroborative genomic data reveal a significant association between non-synonymous variants of and the incidence of colon cancer in humans. Taken together, the results suggest that endogenous CB2 activation suppresses colon tumorigenesis by shifting the balance towards anti-tumor immune cells in mice and thus portray the prognostic value of variants for colon cancer patients.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9961974 | PMC |
| http://dx.doi.org/10.3390/ijms24044060 | DOI Listing |
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