ReviewSmall GTPases2016
Mechano-reciprocity is maintained between physiological boundaries by tuning signal flux through the Rho-associated protein kinase.
Review in Small GTPases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
The trial behind it
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
17 citing papers in PubMed, 52 citations in OpenAlex.
- Compressive stress-driven Piezo1 activation and Rho-ROCK mechanotransduction promote tumor progression via epigenetic mechanical memory.Science advances · 2026Article
- Mechanisms of breast cancer metastasis: the role of extracellular matrix.Molecular and cellular biochemistry · 2025Review
- Novel De NovoInternational journal of molecular sciences · 2025Article
- Article
- Interrelationships between the extracellular matrix and the immune microenvironment that govern epithelial tumour progression.Clinical science (London, England : 1979) · 2022Review
- TAGLN mediated stiffness-regulated ovarian cancer progression via RhoA/ROCK pathway.Journal of experimental & clinical cancer research : CR · 2021Article
- Extracellular Matrices and Cancer-Associated Fibroblasts: Targets for Cancer Diagnosis and Therapy?Cancers · 2021Review
- Viscoelasticity Acts as a Marker for Tumor Extracellular Matrix Characteristics.Frontiers in cell and developmental biology · 2021Review
- Application of low-intensity pulsed therapeutic ultrasound on mesenchymal precursors does not affect their cell properties.PloS one · 2021Article
- Acute compressive stress activates RHO/ROCK-mediated cellular processes.Small GTPases · 2020Article
- ROCK-mediated selective activation of PERK signalling causes fibroblast reprogramming and tumour progression through a CRELD2-dependent mechanism.Nature cell biology · 2020Article
- Cancer-associated fibroblasts: how do they contribute to metastasis?Clinical & experimental metastasis · 2019Review
- Neural Crest Stem-Like Cells Non-genetically Induced from Human Gingiva-Derived Mesenchymal Stem Cells Promote Facial Nerve Regeneration in Rats.Molecular neurobiology · 2018Article
- The mechanical microenvironment regulates ovarian cancer cell morphology, migration, and spheroid disaggregation.Scientific reports · 2018Article
- Charting the unexplored extracellular matrix in cancer.International journal of experimental pathology · 2018Review
- Hyaluronan, Cancer-Associated Fibroblasts and the Tumor Microenvironment in Malignant Progression.Frontiers in cell and developmental biology · 2018Review
- The Role of the Extracellular Matrix and Its Molecular and Cellular Regulators in Cancer Cell Plasticity.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanical properties of the ECM strongly influence the behavior of all cell types within a given tissue. Increased matrix tension promotes epithelial cell proliferation by engaging mitogenic mechanotransduction signaling including the Salvador/Warts/Hippo, PI 3-kinase, Rho, Wnt and MAP kinase pathways. The Rho signaling pathways in particular are capable of increasing intra-cellular tension by elevating the production and contractility of the actomyosin cytoskeleton, which counteracts tension changes within the matrix in a process termed mechano-reciprocity. We have discovered that Rho-ROCK signaling increases the production of ECM through paracrine signaling between the epithelium and fibroblasts and also the remodeling of the ECM by regulating focal adhesion dynamics in fibroblasts. These two phenomena together cause increased ECM tension. Enhanced mechano-reciprocity results in ever-increasing intra- and extra-cellular tension in a vicious cycle that promotes cell proliferation and tumor progression. These insights reveal that inhibiting mechano-reciprocity, reducing ECM tension and targeting cancer-associated fibroblasts in a coordinated fashion has potential as cancer therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.