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Updated: Mar 1, 2026
Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
Published on: March 19, 2019
Candida albicans synergizes with Fusobacterium nucleatum in colorectal cancer progression via the Flo9-RadD
Jialu Li1, Chenyi Zhang2, Xinhua Huang3
1Division of Gastroenterology and Hepatology, Shanghai Institute of Digestive Disease, NHC Key Laboratory of Digestive Diseases, State Key Laboratory of Systems Medicine for Cancer, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200001, China; Shanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Department of Gastroenterology, Center for Immune-Related Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Abstract:
Fusobacterium nucleatum tumor infiltration is a hallmark of colorectal cancer (CRC) progression. However, whether and how other microbes influence F. nucleatum in CRC remains unclear. Here, we discover that the commensal fungus Candida albicans synergizes with F. nucleatum to promote CRC pathogenesis and contributes to poor patient outcomes. Co-inoculation of C. albicans and F. nucleatum accelerates CRC progression compared to either microbe alone in animal models. C. albicans strains isolated from CRC patients exhibiting enhanced hyphal morphogenesis and elevated FLO9 expression promote F. nucleatum-mediated tumor growth. Mechanistically, through the Flo9-RadD interaction, C. albicans facilitates F. nucleatum localization to the colonic mucosa and promotes F. nucleatum-driven malignant transformation. Translationally, we demonstrate that L-arginine disrupts the interaction between C. albicans and F. nucleatum, reducing their synergistic pro-tumor activity in CRC models in vivo. These findings highlight fungal-bacterial interaction as a critical etiologic mechanism in CRC and a potential therapeutic target.
