{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Wenguang Wu"],"species":["Homo Sapiens"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0017040000"],"submitter_email":["wuwenguang08@126.com"],"submitter_affiliation":["Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"additional_accession":[]},"is_claimable":false,"name":"Bacteroides fragilis toxin promotes gallbladder cancer in mice","description":"Enterotoxigenic Bacteroides fragilis (ETBF), which secretes B. fragilis toxin (BFT) and has been associated with colorectal cancer, can be enriched in patients with gallbladder cancer (GBC). Whether and how ETBF contributes to GBC is unclear. Here we confirm using analysis of patient samples that ETBF is enriched in GBC tumors, while experiments in mice show that ETBF colonises the gallbladder. In vitro, and in patient-derived organoids, ETBF promoted GBC proliferation. ETBF also promoted tumor growth in a BFT-dependent manner in a mouse GBC allograft model. Mechanistically, the tumorigenic activity of BFT was dependent upon the ETBF surface protein, MltD, which interacts with the host receptor protein, TMPRSS13. This interaction activated JAK2-STAT3 signaling to promote tumorigenesis. BFT also activated NF-κB signaling, which increased CXCL1 secretion, leading to myeloid-derived suppressor cells recruitment and angiogenesis in the tumor microenvironment. Taken together, these findings uncover mechanisms through which ETBF facilitates GBC development, with potential promise as therapeutic targets to limit GBC progression.","dates":{"publication":"Thu May 07 00:00:00 GMT+01:00 2026"},"accession":"PXD078162","cross_references":{"TAXONOMY":["9606"]}}