Molecular pathways in viral hepatitis-associated liver carcinogenesis: An update

Figure 2 A schematic overview showing the influences of hepatitis B virus and hepatitis C virus proteins on the nuclear factor kappa-Β signaling pathway. Nuclear factor kappa-Β (NF-κB) normally localizes to the cytoplasm and binds to members of the inhibitory IκB family (IκBα, IκBβ, p105, and p100) of proteins, blocking the nuclear translocation of NF-κB. Therefore, deregulation of the IκB family is required for NF-κB to be translocated into the nucleus. Hepatitis B virus and hepatitis C virus use different mechanisms to modulate these transduction pathways by modulating NF-κB proteins activation, interaction with cellular proteins, interaction with other signaling cascades, and ER stress induction. COX-2: Cyclooxygenase-2; ERK: Extracellular signal-regulated kinase; IKK: IκB kinase; IL: Interleukin; JNK: c-Jun N-terminal kinase; p38 MAPK: p38 Mitogen-activated protein kinase; PG: Prostaglandin; ROS: Reactive oxygen species; TNF-α: Tumor necrosis factor-α; TNFR: Tumor necrosis factor receptor; ⊥: Inhibition.