ArticlePloS one2013
How changes in extracellular matrix mechanics and gene expression variability might combine to drive cancer progression.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Evaluation of Metaplastic Triple-Negative Breast Cancer Extracellular Matrix Structure and Protein Composition.Bioengineering (Basel, Switzerland) · 2025Article
- A multiscale chemical-mechanical model predicts impact of morphogen spreading on tissue growth.NPJ systems biology and applications · 2023Article
- A multi-layered hybrid model for cancer cell invasion.Medical & biological engineering & computing · 2022Article
- Versican silencing in BeWo cells and its implication in gestational trophoblastic diseases.Histochemistry and cell biology · 2019Article
- Hydrogel Environment Supports Cell Culture Expansion of a Grade IV Astrocytoma.Neurochemical research · 2017Article
- Endogenous retroviral promoter exaptation in human cancer.Mobile DNA · 2016Review
- Control of cancer formation by intrinsic genetic noise and microenvironmental cues.Nature reviews. Cancer · 2015Review
- Simulating cancer growth with multiscale agent-based modeling.Seminars in cancer biology · 2015Review
- Integrating Multiscale Modeling with Drug Effects for Cancer Treatment.Cancer informatics · 2015Review
- Molecular pathways: not a simple tube--the many functions of blood vessels.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Review
- Pathway and network approaches for identification of cancer signature markers from omics data.Journal of Cancer · 2015Review
- Versican and the regulation of cell phenotype in disease.Biochimica et biophysica acta · 2014Review
- Using real-time impedance-based assays to monitor the effects of fibroblast-derived media on the adhesion, proliferation, migration and invasion of colon cancer cells.Bioscience reports · 2014Article
- 'Particle genetics': treating every cell as unique.Trends in genetics : TIG · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in extracellular matrix (ECM) structure or mechanics can actively drive cancer progression; however, the underlying mechanism remains unknown. Here we explore whether this process could be mediated by changes in cell shape that lead to increases in genetic noise, given that both factors have been independently shown to alter gene expression and induce cell fate switching. We do this using a computer simulation model that explores the impact of physical changes in the tissue microenvironment under conditions in which physical deformation of cells increases gene expression variability among genetically identical cells. The model reveals that cancerous tissue growth can be driven by physical changes in the microenvironment: when increases in cell shape variability due to growth-dependent increases in cell packing density enhance gene expression variation, heterogeneous autonomous growth and further structural disorganization can result, thereby driving cancer progression via positive feedback. The model parameters that led to this prediction are consistent with experimental measurements of mammary tissues that spontaneously undergo cancer progression in transgenic C3(1)-SV40Tag female mice, which exhibit enhanced stiffness of mammary ducts, as well as progressive increases in variability of cell-cell relations and associated cell shape changes. These results demonstrate the potential for physical changes in the tissue microenvironment (e.g., altered ECM mechanics) to induce a cancerous phenotype or accelerate cancer progression in a clonal population through local changes in cell geometry and increased phenotypic variability, even in the absence of gene mutation.
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