ArticleMedical oncology (Northwood, London, England)2026
Antitumor effect of the AP5Z1 small-molecule inhibitor PGG in hepatocellular carcinoma.
Article in Medical oncology (Northwood, London, England), 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
In this study, small-molecule inhibitors targeting AP5Z1 were developed, and their antitumor activity against hepatocellular carcinoma (HCC) and related mechanisms were evaluated. Candidate molecules were initially screened via computer-aided virtual screening, and CCK-8 assays were performed to verify their inhibitory effects on the proliferation of HCC cells. The interactions between compounds and targets were confirmed using techniques such as docking simulations, dynamics analyses on a molecular level, cellular thermal shift assays (CETSAs)and Surface Plasmon Resonance(SPR). In vitro cellular experiments, including colony formation, flow cytometric apoptosis detection, Western blotting, and dual-fluorescent autophagy systems, were performed to assess how pentagalloylglucose (PGG) modulates the malignant phenotypes of HCC. A subcutaneous xenograft model was constructed using nude mice to analyze the suppressive effect of PGG on tumor growth in vivo. Through virtual screening and activity validation, PGG was identified as the core candidate molecule. PGG stably binds to the predicted binding pocket of AP5Z1, forming an extensive hydrogen bond network. In vitro tests showed that PGG inhibits the proliferation of HCC cells and induces their apoptosis, accompanied by changes in autophagy-related markers. The results of in vivo experiments confirmed that PGG significantly decreases the volume and weight of tumors, decreases the expression of AP5Z1 and Ki67, and increases the levels of markers associated with apoptosis and autophagy. PGG acts by inhibiting AP5Z1-mediated ubiquitination and degradation of the tumor suppressor PTEN, thereby blocking the downstream PI3K/AKT/mTOR signaling pathway. Pentagalloylglucose (PGG) acts as an orally available small-molecule inhibitor targeting AP5Z1 and suppresses the progression of HCC both in vitro and in vivo by regulating the ubiquitination of PTEN and downstream signaling cascades. These findings indicate that PGG is a novel candidate for targeted therapy.
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