Fig. 9

Schematic representation of the mechanism by which HERC2 promotes inflammation-related HCC progression. Inflammatory stimulation induces HERC2 expression in hepatocytes. HERC2 interacts with the C-terminal of PTP1B and limits PTP1B translocation in ER-plasma membrane junctions, thereby inhibiting PTP1B-mediated dephosphorylation of JAK2. The enhanced JAK2 phosphorylation activates STAT3 phosphorylation. Consequently, the overactivation of STAT3 is correlated with increased expression of stemness-related genes and PD-L1, further promoting cancer stemness and immune evasion in HCC