ArticleTheranostics2026
A peptide-based PROTAC targeting FOXM1 suppresses fibrosis-associated hepatocarcinogenesis.
Article in Theranostics, 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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15 authors.
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Abstract
Background: Liver fibrosis is not only a major cause of cirrhosis but also an important risk factor for hepatocellular carcinoma (HCC). Currently, few drugs can effectively reverse established liver fibrosis. FOXM1, a transcription factor aberrantly activated in chronic liver disease, has been implicated in fibrosis-associated hepatocarcinogenesis. Nevertheless, effective pharmacological strategies for targeting FOXM1 are still lacking. Methods: We developed peptide-based proteolysis-targeting chimeras (PROTACs) by conjugating the FOXM1-binding peptide P49 with different E3 ligase ligands. Among them, P49-PROTAC Results: Mechanistically, P49-PROTAC Conclusions: The FOXM1-ADAMTS12 axis may represent an important molecular link between liver fibrosis and hepatocarcinogenesis. Targeting FOXM1 with peptide-based PROTACs may provide a promising therapeutic strategy to attenuate liver fibrosis and suppress HCC development.
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