上海交通大学医学院房静远研究组宣布他们探明了白色念珠菌与核梭杆菌通过Flo9-RadD相互作用在结直肠癌进展中协同作用。相关论文发表在2026年2月26日出版的《癌细胞》杂志上。

该研究团队发现共生真菌白色念珠菌与具核念珠菌协同促进结直肠癌的发病机制，并导致患者预后不良。在动物模型中，与单独接种白色念珠菌和具核梭菌相比，共同接种可加速结直肠癌的进展。从结直肠癌患者中分离出的白色念珠菌菌丝形态发生增强，FLO9表达升高，可促进核念珠菌介导的肿瘤生长。机制上，通过Flo9-RadD相互作用，白色念珠菌促进具核梭菌定位到结肠粘膜，促进具核梭菌驱动的恶性转化。从转化的角度来看，研究团队证明L-精氨酸破坏白色念珠菌和具核梭菌之间的相互作用，降低它们在CRC模型中的协同促肿瘤活性。这些发现强调了真菌-细菌相互作用是结直肠癌的关键病因机制和潜在的治疗靶点。

据悉，核热杆菌肿瘤浸润是结直肠癌（CRC）进展的标志。然而，其他微生物是否以及如何影响结直肠癌中的具核梭菌仍不清楚。

附：英文原文

Title: Candida albicans synergizes with Fusobacterium nucleatum in colorectal cancer progression via the Flo9-RadD interaction

Author: Jialu Li, Chenyi Zhang, Xinhua Huang, Hongxiang Sun, Lei Yang, Hongzhi Liu, Lu Zhang, Ningbo Wu, Yuanhong Xie, Jingjing Qi, Xiaoxu Leng, Yun Cui, Song Li, Ziran Kang, Zhuolei Kou, Ning-Ning Liu, Pengfei Lan, Beilei Xuan, Dengfeng Cao, Guo-Xiang Cai, Yingxuan Chen, Jianfeng Chen, Zhaoyuan Liu, Florent Ginhoux, Changbin Chen, Bing Su, Jing-Yuan Fang

Issue&Volume: 2026-02-26

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.

DOI: 10.1016/j.ccell.2026.02.001

Source: https://www.cell.com/cancer-cell/abstract/S1535-6108(26)00100-5