Antiviral therapy for hepatitis B virus infection is beneficial for the prognosis hepatocellular carcinoma

Figure 2 The pathogenesis of liver cancer. The occurrence of hepatocellular carcinoma is related to the abnormal activation of multiple signaling pathways. When there is a wnt signal, abnormalities in the AXIN gene can inhibit β-catenin degradation, accumulating in the cytoplasm and entering the nucleus to bind with T-cell factor family proteins, enhancing downstream gene transcription. In the presence of hedgehog (Hh) ligands, the binding of Hh ligand to patched (Ptch)-1 can lead to the endocytosis of Ptch-1, thereby relieving the inhibition of smoothened (Smo). The accumulation and activation of Smo lead to the dissociation of suppressor of fused and GLI, forming GLI activators that promote the expression of target genes. Notch protein is cleaved by furin like proteins and expressed on the cell surface in the form of heterodimers. After binding with ligands, it is cleaved by proteases, and then cleaved by γ-secretase complex in the transmembrane region. At this time, the activated molecule notch intracellular domain enters the nucleus to regulate the transcription of target genes. Hh: Hedgehog; Smo: Smoothened; TCF/LEF: Transcription factor T-cell factor/lymphoid enhancer factor.