ArticleProceedings of the National Academy of Sciences of the United States of America2025
Intercellular contractile force attenuates chemosensitivity through Notch-MVP-mediated nuclear drug export.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Cancer drug response and resistance: molecular mechanisms and combating strategies.Signal transduction and targeted therapy · 2026Review
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- Piezo1 Channel Mediates Mechanically Programmable Drug Delivery to Potentiate Intravesical Chemotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transformative biomechanics and mechanobiology breakthroughs shaping the future of health and medicine.Innovation (Cambridge (Mass.)) · 2026Review
- Integrative Multi-Omics and Experimental Analyses Identify TAPBP as a Key Mediator Linking Genetic Susceptibility to Melanocyte Dysfunction in Vitiligo.Clinical, cosmetic and investigational dermatology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Resistance to chemotherapeutics is one major challenge to clinical effectiveness of cancer treatment and is primarily interpreted by various biochemical mechanisms. This study establishes an inverse correlation between tumor cell contractility and chemosensitivity. In both clinical biopsies and cancer cell lines, high/low actomyosin-mediated contractile force attenuates/enhances the vulnerability to chemotherapy, which depends on intercellular force propagation. Cell-cell interaction force activates the mechanosensitive Notch signaling that upregulates the downstream effector major vault protein, which facilitates the export of chemotherapy drugs from nuclei, leading to the reduction of chemosensitivity. Cellular contractility promotes the tolerance of tumor xenografts to chemotherapy and sustains tumor growth in vivo, which can be reversed by the inhibition of contractile force, Notch signaling, or major vault protein. Further, the actomyosin-Notch signaling is associated with drug resistance and cancer recurrence of patients. These findings unveil a regulatory role of intercellular force in chemosensitivity, which could be harnessed as a promising target for cancer mechanotherapeutics.
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Registered trials
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