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<p>Colitis-associated cancer (CAC) is a serious complication of inflammatory bowel disease (IBD). Recent evidence has indicated that <i>Fusobacterium nucleatum</i> (<i>F. nucleatum</i>) may promote intestinal inflammation and carcinogenesis. However, the effects of <i>F. nucleatum</i> on the cancerous transformation of IBD, along with its underlying mechanisms, remain poorly understood. Our findings revealed that <i>F. nucleatum</i> 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 <i>F. nucleatum</i> modulated nicotinamide (NAM) metabolism to promote the proliferation of CAC. Mechanistically, <i>F. nucleatum</i> upregulated NNMT to increase PARP1 expression, thereby activating MAPK signalling pathway. These findings provide insight into <i>F. nucleatum</i>-induced metabolic dysregulation and inflammatory cancer development and may propose novel intervention strategies for the prevention and treatment of microbial-associated inflammatory carcinogenesis.</p>

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Fusobacterium nucleatum regulates nicotinamide metabolism via the upregulation of NNMT to activate PARP1/MAPK signalling in colitis-associated cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月30日

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  • Jing Lei,
  • Peiyu Yang,
  • Feng Xu,
  • Wenhao Su,
  • Zihao Liu,
  • Juan Li,
  • Siyuan Chen,
  • Yongyu Chen

摘要

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.