ArticleNature communications2024
An allosteric inhibitor of RhoGAP class-IX myosins suppresses the metastatic features of cancer cells.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Salvianolic acid monomers against metastasis: Decoding the multilayered interception of EMT, angiogenesis and immune evasion (Review).International journal of molecular medicine · 2026Review
- Long-tailed class I myosins rely on tail-mediated phosphoinositide recognition for specific membrane recruitment.Cell communication and signaling : CCS · 2025Article
- Molecular Docking and Target-Specific Binding Profiles of Benzosuberane-Based Compounds.ChemMedChem · 2025Review
- The Allosteric Inhibitor Pentachloropseudilin Inhibits Myosin 1C ATPase Activity and Recapitulates Retinitis Pigmentosa Phenotypes in Mice.ACS omega · 2025Article
Corrections and comments
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Authors and funding
32 authors.
Funding
Abstract
Aberrant Ras homologous (Rho) GTPase signalling is a major driver of cancer metastasis, and GTPase-activating proteins (GAPs), the negative regulators of RhoGTPases, are considered promising targets for suppressing metastasis, yet drug discovery efforts have remained elusive. Here, we report the identification and characterization of adhibin, a synthetic allosteric inhibitor of RhoGAP class-IX myosins that abrogates ATPase and motor function, suppressing RhoGTPase-mediated modes of cancer cell metastasis. In human and murine adenocarcinoma and melanoma cell models, including three-dimensional spheroid cultures, we reveal anti-migratory and anti-adhesive properties of adhibin that originate from local disturbances in RhoA/ROCK-regulated signalling, affecting actin-dynamics and actomyosin-based cell-contractility. Adhibin blocks membrane protrusion formation, disturbs remodelling of cell-matrix adhesions, affects contractile ring formation, and disrupts epithelial junction stability; processes severely impairing single/collective cell migration and cytokinesis. Combined with the non-toxic, non-pathological signatures of adhibin validated in organoids, mouse and Drosophila models, this mechanism of action provides the basis for developing anti-metastatic cancer therapies.
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Registered trials
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