Matrix Rigidity Regulates Cancer Cell Growth and Cellular Phenotype

Background The mechanical properties of the extracellular matrix have an important role in cell growth and differentiation. However, it is unclear as to what extent cancer cells respond to changes in the mechanical properties (rigidity/stiffness) of the microenvironment and how this response varies among cancer cell lines. Methodology/Principal Findings In this study we used a recently developed 96-well plate system that arrays extracellular matrix-conjugated polyacrylamide gels that increase in stiffness by at least 50-fold across the plate. This plate was used to determine how changes in the rigidity of the extracellular matrix modulate the biological properties of tumor cells. The cell lines tested fall into one of two categories based on their proliferation on substrates of differing stiffness: “rigidity dependent” (those which show an increase in cell growth as extracellular rigidity is increased), and “rigidity independent” (those which grow equally on both soft and stiff substrates). Cells which grew poorly on soft gels also showed decreased spreading and migration under these conditions. More importantly, seeding the cell lines into the lungs of nude mice revealed that the ability of cells to grow on soft gels in vitro correlated with their ability to grow in a soft tissue environment in vivo. The lung carcinoma line A549 responded to culture on soft gels by expressing the differentiated epithelial marker E-cadherin and decreasing the expression of the mesenchymal transcription factor Slug. Conclusions/Significance These observations suggest that the mechanical properties of the matrix environment play a significant role in regulating the proliferation and the morphological properties of cancer cells. Further, the multiwell format of the soft-plate assay is a useful and effective adjunct to established 3-dimensional cell culture models.

[1]  Timothy J Gardner,et al.  Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance. , 2007, American journal of physiology. Heart and circulatory physiology.

[2]  Buzz Baum,et al.  Transitions between epithelial and mesenchymal states in development and disease. , 2008, Seminars in cell & developmental biology.

[3]  J. Parsons,et al.  Focal adhesion kinase as a regulator of cell tension in the progression of cancer. , 2008, Seminars in cancer biology.

[4]  K. Mostov,et al.  From cells to organs: building polarized tissue , 2008, Nature Reviews Molecular Cell Biology.

[5]  S. Thomson,et al.  Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions , 2008, Clinical & Experimental Metastasis.

[6]  D. Discher,et al.  Extracellular matrix elasticity directs stem cell differentiation. , 2007, Journal of musculoskeletal & neuronal interactions.

[7]  C. Heldin,et al.  Signaling networks guiding epithelial–mesenchymal transitions during embryogenesis and cancer progression , 2007, Cancer science.

[8]  J. Beaulieu,et al.  Integrin-linked kinase regulates migration and proliferation of human intestinal cells under a fibronectin-dependent mechanism , 2010, Journal of cellular physiology.

[9]  W. Burns,et al.  Connective Tissue Growth Factor and Cardiac Fibrosis after Myocardial Infarction , 2005, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[10]  J. Haley,et al.  Loss of homotypic cell adhesion by epithelial-mesenchymal transition or mutation limits sensitivity to epidermal growth factor receptor inhibition , 2007, Molecular Cancer Therapeutics.

[11]  Y. Wang,et al.  Preparation of a flexible, porous polyacrylamide substrate for mechanical studies of cultured cells. , 1998, Methods in enzymology.

[12]  G. Christofori,et al.  The role of the cell-adhesion molecule E-cadherin as a tumour-suppressor gene. , 1999, Trends in biochemical sciences.

[13]  Adam J Engler,et al.  Embryonic cardiomyocytes beat best on a matrix with heart-like elasticity: scar-like rigidity inhibits beating , 2008, Journal of Cell Science.

[14]  Michael P. Sheetz,et al.  Differential Matrix Rigidity Response in Breast Cancer Cell Lines Correlates with the Tissue Tropism , 2009, PloS one.

[15]  S. Sen,et al.  Matrix Elasticity Directs Stem Cell Lineage Specification , 2006, Cell.

[16]  Lisa A Flanagan,et al.  Neurite branching on deformable substrates , 2002, Neuroreport.

[17]  Paul A. Janmey,et al.  Cell-Cycle Control by Physiological Matrix Elasticity and In Vivo Tissue Stiffening , 2009, Current Biology.

[18]  R. Assoian,et al.  Growth control by intracellular tension and extracellular stiffness. , 2008, Trends in cell biology.

[19]  Jayanta Debnath,et al.  Morphogenesis and oncogenesis of MCF-10A mammary epithelial acini grown in three-dimensional basement membrane cultures. , 2003, Methods.

[20]  K. Janssen,et al.  Epithelial morphogenesis and intestinal cancer: new insights in signaling mechanisms. , 2008, Advances in cancer research.

[21]  R. Weinberg,et al.  Integrin β1-focal adhesion kinase signaling directs the proliferation of metastatic cancer cells disseminated in the lungs , 2009, Proceedings of the National Academy of Sciences.

[22]  R. Foisner,et al.  E-cadherin regulates cell growth by modulating proliferation-dependent β-catenin transcriptional activity , 2001, The Journal of cell biology.

[23]  H. Kanetake,et al.  Calreticulin Represses E-cadherin Gene Expression in Madin-Darby Canine Kidney Cells via Slug* , 2006, Journal of Biological Chemistry.

[24]  M. Dembo,et al.  Substrate flexibility regulates growth and apoptosis of normal but not transformed cells. , 2000, American journal of physiology. Cell physiology.

[25]  Sanjay Kumar,et al.  The mechanical rigidity of the extracellular matrix regulates the structure, motility, and proliferation of glioma cells. , 2009, Cancer research.

[26]  D. E. Discher,et al.  Matrix elasticity directs stem cell lineage — Soluble factors that limit osteogenesis , 2009 .

[27]  Cynthia A. Reinhart-King,et al.  Tensional homeostasis and the malignant phenotype. , 2005, Cancer cell.

[28]  Mikala Egeblad,et al.  Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin Signaling , 2009, Cell.

[29]  Adam J. Engler,et al.  Myotubes differentiate optimally on substrates with tissue-like stiffness , 2004, The Journal of cell biology.

[30]  Alan Hall,et al.  Rho GTPases: biochemistry and biology. , 2005, Annual review of cell and developmental biology.

[31]  Radhika Desai,et al.  ROCK-generated contractility regulates breast epithelial cell differentiation in response to the physical properties of a three-dimensional collagen matrix , 2003, The Journal of cell biology.

[32]  D. Discher,et al.  Cell responses to the mechanochemical microenvironment--implications for regenerative medicine and drug delivery. , 2007, Advanced drug delivery reviews.

[33]  Donald E Ingber,et al.  Cell tension, matrix mechanics, and cancer development. , 2005, Cancer cell.

[34]  Kevin W. Eliceiri,et al.  Matrix density-induced mechanoregulation of breast cell phenotype, signaling, and gene expression through a FAK-ERK linkage , 2009, Oncogene.