Fig. 7: During hepatic fibrosis, TGF-β-activated Akt phosphorylates Nur77 to induce its degradation in HSCs, leading to the suppressed expression of depalmitoylase ABHD17B, a downstream target gene of Nur77. | Nature Metabolism

Fig. 7: During hepatic fibrosis, TGF-β-activated Akt phosphorylates Nur77 to induce its degradation in HSCs, leading to the suppressed expression of depalmitoylase ABHD17B, a downstream target gene of Nur77.

From: HK1 from hepatic stellate cell–derived extracellular vesicles promotes progression of hepatocellular carcinoma

Fig. 7

The palmitoylation of HK1 is thus elevated, which promotes HK1 translocation to the plasma membrane for subsequent secretion via lEVs. The HSC-derived lEV HK1 is hijacked by HCC cells, which facilitates the reprogramming of glycolysis to promote HCC progression. Compound PDNPA antagonizes TGF-β-induced Nur77 degradation and inhibits HK1 secretion, thereby effectively repressing HCC progression.

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