ArticleMolecular biology of the cell1997
Rho-stimulated contractility contributes to the fibroblastic phenotype of Ras-transformed epithelial cells.
Article in Molecular biology of the cell, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 162 citations in OpenAlex.
- Exploiting differential effects of actomyosin contractility to control cell sorting among breast cancer cells.Molecular biology of the cell · 2021Article
- Generation of anisotropic strain dysregulates wild-type cell division at the interface between host and oncogenic tissue.Current biology : CB · 2021Article
- The Expression of the Cancer-Associated lncRNAInternational journal of molecular sciences · 2021Article
- The Myosin Family of Mechanoenzymes: From Mechanisms to Therapeutic Approaches.Annual review of biochemistry · 2020Review
- The Regulation of Intestinal Mucosal Barrier by Myosin Light Chain Kinase/Rho Kinases.International journal of molecular sciences · 2020Review
- ILK supports RhoA/ROCK-mediated contractility of human intestinal epithelial crypt cells by inducing the fibrillogenesis of endogenous soluble fibronectin during the spreading process.BMC molecular and cell biology · 2020Article
- Article
- Non-muscle myosin II in disease: mechanisms and therapeutic opportunities.Disease models & mechanisms · 2015Review
- Validation of the effects of TGF-β1 on tumor recurrence and prognosis through tumor retrieval and cell mechanical properties.Cancer cell international · 2014Article
- Article
- Cadherins in collective cell migration of mesenchymal cells.Current opinion in cell biology · 2012Review
- From mechanical force to RhoA activation.Biochemistry · 2012Review
- Integrins and cadherins join forces to form adhesive networks.Journal of cell science · 2011Review
- Forcing form and function: biomechanical regulation of tumor evolution.Trends in cell biology · 2011Review
- Downregulation of metastasis suppressor 1(MTSS1) is associated with nodal metastasis and poor outcome in Chinese patients with gastric cancer.BMC cancer · 2010Article
- Vinculin potentiates E-cadherin mechanosensing and is recruited to actin-anchored sites within adherens junctions in a myosin II-dependent manner.The Journal of cell biology · 2010Article
- Dual FGF-2 and intergrin alpha5beta1 signaling mediate GRAF-induced RhoA inactivation in a model of breast cancer dormancy.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2009Article
- Restoration of E-cadherin cell-cell junctions requires both expression of E-cadherin and suppression of ERK MAP kinase activation in Ras-transformed breast epithelial cells.Neoplasia (New York, N.Y.) · 2008Article
- Resensitization of breast cancer cells to anoikis by tropomyosin-1: role of Rho kinase-dependent cytoskeleton and adhesion.Oncogene · 2005Article
- Integrin-dependent actomyosin contraction regulates epithelial cell scattering.The Journal of cell biology · 2005Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oncogenic transformation of cells alters their morphology, cytoskeletal organization, and adhesive interactions. When the mammary epithelial cell line MCF10A is transformed by activated H-Ras, the cells display a mesenchymal/fibroblastic morphology with decreased cell-cell junctions but increased focal adhesions and stress fibers. We have investigated whether the transformed phenotype is due to Rho activation. The Ras-transformed MCF10A cells have elevated levels of myosin light chain phosphorylation and are more contractile than their normal counterparts, consistent with the activation of Rho. Furthermore, inhibitors of contractility restore a more normal epithelial phenotype to the Ras-transformed MCF10A cells. However, inhibiting Rho by microinjection of C3 exotransferase or dominant negative RhoA only partially restores the normal phenotype, in that it fails to restore normal junctional organization. This result prompted us to examine the effect that inhibiting Rho would have on the junctions of normal MCF10A cells. We have found that inhibiting Rho by C3 microinjection leads to a disruption of E-cadherin cytoskeletal links in adherens junctions and blocks the assembly of new adherens junctions. The introduction of constitutively active Rho into normal MCF10A cells did not mimic the Ras-transformed phenotype. Thus, these results lead us to conclude that some, but not all, characteristics of Ras-transformed epithelial cells are due to activated Rho. Whereas Rho is needed for the assembly of adherens junctions, high levels of activated Rho in Ras-transformed cells contribute to their altered cytoskeletal organization. However, additional events triggered by Ras must also be required for the disruption of adherens junctions and the full development of the transformed epithelial phenotype.
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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.