fig1

Figure 1. Mechanisms by which two tumor-resident microbes promote HCC progression by modulating host oncogenic pathways. (A) Direct binding-mediated pathway activation. K. pneumoniae binds to HCC cells via PBP1B and activates the TLR4/NF-κB signaling pathway, leading to inflammation, cell survival, proliferation, and ultimately tumorigenesis; (B) Secreted metabolite-mediated pathway activation. C. mitsuokai surface proteins Gtr1/RagA bind to the γ-catenin receptor on HCC cells, leading to tumor colonization. It secretes quinolinic acid to activate the PI3K/AKT signaling pathway by binding to TIE2, influencing cell survival and proliferation. HCC: Hepatocellular carcinoma; PBP1B: penicillin-binding protein 1B; TLR4: toll-like receptor 4; MyD88: myeloid differentiation primary response protein 88; NF-κB: nuclear factor kappa-B; PI3K: phosphatidylinositol 3-kinase; AKT: protein kinase B.