Fig. 5

EBV-induced oncogenesis through the TGF-β signaling pathway. After TGF-β is stimulated, it activates Smad2 and Smad3 and then combines with Smad4 to enter the nucleus to regulate transcription, inhibit cell proliferation signals, and promote apoptosis of injured cells. LMP2A and EBNA1 can destabilize Smad2, thereby inhibiting the proliferation-inhibiting signal produced by TGF-β. Cells that have been infected with EBV can promote the activation of the TGF-β signaling pathway and increase the expression of the BZLF1 gene, leading to increased viral replication and enhanced infectivity of EBV