ArticleJournal of hepatocellular carcinoma2025
Taurine-Modified Gossypol Exerts Dual Anti-Hepatocellular Carcinoma Effects by Inactivating PI3K/AKT Pathway and Targeting FASN-Mediated Lipid Metabolism in Regulatory T Cells.
Article in Journal of hepatocellular carcinoma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Hepatocellular carcinoma (HCC) remains a highly challenging malignancy to treat with a dismal prognosis. The immunosuppressive tumor microenvironment (TIME), particularly regulatory T cells (Tregs), is a key driver of treatment resistance. This study aimed to investigate the anti-tumor efficacy and underlying mechanism of taurine-modified gossypol (GT)-a novel conjugate derived from two natural products (taurine and gossypol) with potential synergistic activity. Methods: The anti-proliferative (CCK-8 assay), pro-apoptotic (Annexin V/PI staining) and cell cycle-regulatory (PI staining) effects of GT were evaluated in HepG2 cells and patient-derived HCC organoids. scRNA-seq and multiparametric flow cytometry were used to analyze alterations in the TIME. Molecular docking and surface plasmon resonance (SPR) were performed to validate the binding affinity (KD) between GT and FASN. Western blotting assessed PI3K/AKT and lipid metabolism pathways. Results: GT dose-dependently inhibited HCC proliferation, induced apoptosis and caused G1 arrest, with concomitant PI3K/AKT pathway suppression. scRNA-seq revealed a selective reduction in Treg proportion following GT treatment. Mechanistically, GT bound to FASN with high affinity, inhibiting its activity and disrupting lipid metabolism in Tregs, thereby reprogramming Treg differentiation and function. In HCC patients, a clinically significant link was observed between high levels of FASN expression and reduced survival, based on an analysis of TCGA data. Conclusion: GT exerts synergistic anti-HCC effects through a dual mechanism: directly suppressing tumor proliferation by inactivating the PI3K/AKT pathway, and remodeling the TIME by targeting FASN-dependent lipid metabolism in Tregs. These findings highlight the potential of GT as a novel multitargeted agent for HCC treatment.
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