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A model of HBx promoting venous metastasis of primary liver cancer. HBx promotes the activation of STAT3, which inhibits miR-34a expression. The inhibited miR-34a released its down-regulation of NF-κB, which promotes the expression of HMGB1. On the other hand, HMGB1 secreted extracellularly activates the IL-6/STAT3/miR-34a axis, and positive feedback promotes the secretion of HMGB1. Finally, induced HMGB1 leads to the formation of liver cancer PVTT by promoting EMT and angiogenesis.
