ArticleCancer cell international2025
Fusobacterium nucleatum increases CTGF expression through TLR2-YAP signaling axis in cancer-associated fibroblasts, thereby promoting colorectal cancer progression.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Review
- Intratumoral Microorganisms in Tumors: Current Understanding and Emerging Therapeutic Strategies.MedComm · 2026Review
- From inflammation to fibrosis and cancer: the emerging role of AIEC-derived metabolites in intestinal disease progression.Experimental & molecular medicine · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
Fusobacterium nucleatum (F. nucleatum) is increasingly recognized as a microbial driver of colorectal cancer (CRC) progression through immune modulation, inflammation dysregulation, and activation of oncogenic signaling cascades. Cancer-associated fibroblasts (CAFs), the predominant stromal constituents within the tumor microenvironment (TME), play pivotal roles in orchestrating tumorigenic processes. While F. nucleatum's interactions with epithelial and immune compartments have been extensively characterized, its immunological crosstalk with CAFs remains elusive. Through multimodal experimental approaches including RNA sequencing and functional validation in xenograft models, we delineate a novel TLR2/YAP/CTGF signaling axis mediating F. nucleatum-driven CAFs activation. Specifically, F. nucleatum colonization induces TLR2-dependent YAP dephosphorylation, facilitating its nuclear translocation and transactivation of CTGF, a classic regulator of stromal-tumor crosstalk. Clinically, elevated CTGF expression correlates with F. nucleatum burden in human CRC specimens. These findings position CTGF as a potential therapeutic target in microbiota-driven colorectal carcinogenesis.
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