Mechanotransduction in tumor progression: The dark side of the force
Open accessAbstract
Cancer has been characterized as a genetic disease, associated with mutations that cause pathological alterations of the cell cycle, adhesion, or invasive motility. Recently, the importance of the anomalous mechanical properties of tumor tissues, which activate tumorigenic biochemical pathways, has become apparent. This mechanical induction in tumors appears to consist of the destabilization of adult tissue homeostasis as a result of the reactivation of embryonic developmental mechanosensitive pathways in response to pathological mechanical strains. These strains occur in many forms, for example, hypervascularization in late tumors leads to high static hydrodynamic pressure that can promote malignant progression through hypoxia or anomalous interstitial liquid and blood flow. The high stiffness of tumors directly induces the mechanical activation of biochemical pathways enhancing the cell cycle, epithelial–mesenchymal transition, and cell motility. Furthermore, increases in solid-stress pressure associated with cell hyperproliferation activate tumorigenic pathways in the healthy epithelial cells compressed by the neighboring tumor. The underlying molecular mechanisms of the translation of a mechanical signal into a tumor inducing biochemical signal are based on mechanically induced protein conformational changes that activate classical tumorigenic signaling pathways. Understanding these mechanisms will be important for the development of innovative treatments to target such mechanical anomalies in cancer.
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A growing literature on mechanotransduction suggests that normal or shear strain may be a major determinant of cellular responses.
“Indeed, a growing literature on mechanotransduction, mostly in the cancer field, suggests that normal or shear strain may be a major determinant of cellular responses [27].”
From Fascia Mobility, Proprioception, and Myofascial Pain. (2021) · cites this paper as [27]
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- Authors
- Broders-Bondon, F., Nguyen Ho-Bouldoires, T. H., Fernandez-Sanchez, M.-E., & Farge, E.
- Affiliations
- Mechanics and Genetics of Embryonic and Tumor Development Group, Institut Curie, PSL Research University, Centre National de la Recherche Scientifique, UMR168, Inserm, Sorbonne Universities, Paris, France
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Farge, Emmanuel
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2018-02-21
- Volume
- 217
- Issue
- 5
- Pages
- 1571-1587
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC5940296
- OpenAlex
- W2789065958
- Cited by
- 319
- References
- 188
- Citations by year
- 2026: 21 · 2025: 28 · 2024: 41 · 2023: 37 · 2022: 52 · 2021: 52 · 2020: 43 · 2019: 32 · 2018: 13
- FWCI
- 3.93
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Institut National du Cancer (PLBIO13-172)
- Foundation pour la Recherche Médicale (DEQ20150331702)
- Agence Nationale de la Recherche (16CE14002801)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Keywords
- mechanotransduction, tumor progression, tumor stiffness, tumor hypervascularization, hydrodynamic pressure, solid stress, epithelial-mesenchymal transition, cell motility, cell cycle, protein conformational change, tumor microenvironment
- MeSH terms
- Animals, Extracellular Matrix, Humans, Models, Biological, Neoplasms, Disease Progression, Mechanotransduction, Cellular, Carcinogenesis
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