Fig. 5

Oncogenic mechanisms of EBV in gastric cancer. a EBV induces genomic instability by promoting DNA methylation and inhibiting P53-mediated DNA repair. b EBV-encoded proteins disrupt the TGF-β1/Smad pathway, activate NF-κB and STAT3 signaling pathways, upregulate oncogene expression, and promote the degradation of tumor suppressor proteins, resulting in malignant cell proliferation. c EBV promotes immune evasion by impairing antigen presentation, increasing PD-L1 expression, and disrupting the function of CTLs and NK cells while increasing Tregs and TAMs in the TME. d EBV facilitates angiogenesis via KHSRP/VHL/HIF-1α/VEGFA and PI3K/AKT/mTOR/HIF-1α pathways and enhances extracellular matrix remodeling, aiding metastasis. Red text: EBV components; Black text: host cell components; Direct oncogenesis: a, b; Indirect oncogenesis: c, d. This figure was created with BioRender.com