Fig. 7

Oncogenic mechanisms of EBV in nasopharyngeal carcinoma. a Progression of NPC caused by EBV. b EBV induces genetic instability through inhibition of DNA repair, increased DNA methylation, chromosomal breaks at 11q23, and telomere elongation. c EBV promotes cell proliferation by activating NF-κB, Hedgehog, mTOR signaling pathways. d EBV accelerates G1/S progression in host cells by downregulating GSK3β expression, promoting degradation of p18, and activating the JAK2/STAT3 signaling pathway. e EBV infection promotes anti-apoptotic protein expression, inactivates pro-apoptotic proteins, reduces fumarate hydratase (FH) activity, and inhibits ferroptosis through the p62-Keap1-NRF2 pathway. f EBV evades immune surveillance by modulating PD-L1, MIC-A/B, and B7-H3 expression, and induces lactate, creatinine, and cytokine release, which recruits Treg cells and expands myeloid-derived suppressor cells (MDSCs), creating an immunosuppressive microenvironment. g EBV proteins promote cytokine/chemokine release, inhibit monocyte recruitment, induce TAM, and enhance mitochondrial activity via ROS suppression. h EBV-encoded proteins activate ANXA3-HIF-1α-VEGF and PI3K/AKT/mTOR/HIF-1α pathways to promote angiogenesis. i EBV stimulates glycolysis, increases glutamine uptake, and inhibits lipid degradation via the mTORC1/NF-κB and HIF-1α pathways. Red text: EBV components; Black text: host cell components; Direct oncogenesis: b–e; Indirect oncogenesis: f–i. This figure was created with BioRender.com