Journal Article Review Epublish 3 citations
PubMed: 40411629 DOI: 10.1007/s12672-025-02742-6
Clostridium difficile as a potent trigger of colorectal carcinogenesis.
Discov Oncol 16(1):910
Authors: Javad Nezhadi, Masoud Lahouty, Mohammad Ahangarzadeh Rezaee, Manouchehr Fadaee
Affiliations
- Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
- Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
- Pediatric Health Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
- Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
Clostridium difficile, traditionally recognized as a cause of antibiotic-associated colitis, has emerged as a potential oncogenic factor in colorectal cancer (CRC). This article explores the mechanisms by which C. difficile toxins, TcdA and TcdB, contribute to CRC pathogenesis through epithelial barrier disruption, DNA damage, and chronic inflammation via NF-κB and STAT3 activation. Dysbiosis further exacerbates tumorigenesis by altering microbial metabolites. Understanding these interactions highlights potential therapeutic strategies, including toxin-neutralizing antibodies, fecal microbiota transplantation, and anti-inflammatory interventions, to mitigate CRC risk associated with C. difficile.
MeSH
Clostridium, Clostridioides Difficile, Carcinogenesis