ArticleCellular and molecular life sciences : CMLS2026
Fusobacterium nucleatum regulates nicotinamide metabolism via the upregulation of NNMT to activate PARP1/MAPK signalling in colitis-associated cancer.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Colitis-associated cancer (CAC) is a serious complication of inflammatory bowel disease (IBD). Recent evidence has indicated that Fusobacterium nucleatum (F. nucleatum) may promote intestinal inflammation and carcinogenesis. However, the effects of F. nucleatum on the cancerous transformation of IBD, along with its underlying mechanisms, remain poorly understood. Our findings revealed that F. nucleatum was enriched in 57.1% of CAC tissues, which was higher than that in ulcerative colitis (UC, 53.0%), Crohn's disease (CD, 55.6%), and colorectal cancer (CRC, 53.7%) tissues. Furthermore, we demonstrated that F. nucleatum modulated nicotinamide (NAM) metabolism to promote the proliferation of CAC. Mechanistically, F. nucleatum upregulated NNMT to increase PARP1 expression, thereby activating MAPK signalling pathway. These findings provide insight into F. nucleatum-induced metabolic dysregulation and inflammatory cancer development and may propose novel intervention strategies for the prevention and treatment of microbial-associated inflammatory carcinogenesis.
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