A combinatorial extracellular matrix platform identifies cell-extracellular matrix interactions that correlate with metastasis

Nathan E. Reticker-Flynn, David F. Braga Malta, Monte M. Winslow, John M. Lamar, Mary J. Xu, Gregory H. Underhill, Richard O. Hynes, Tyler E. Jacks and Sangeeta N. Bhatia ()
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Nathan E. Reticker-Flynn: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
David F. Braga Malta: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Monte M. Winslow: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
John M. Lamar: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Mary J. Xu: Massachusetts Institute of Technology
Gregory H. Underhill: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Richard O. Hynes: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Tyler E. Jacks: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Sangeeta N. Bhatia: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology

Nature Communications, 2012, vol. 3, issue 1, 1-12

Abstract: Abstract Extracellular matrix interactions have essential roles in normal physiology and many pathological processes. Although the importance of extracellular matrix interactions in metastasis is well documented, systematic approaches to identify their roles in distinct stages of tumorigenesis have not been described. Here we report a novel-screening platform capable of measuring phenotypic responses to combinations of extracellular matrix molecules. Using a genetic mouse model of lung adenocarcinoma, we measure the extracellular matrix-dependent adhesion of tumour-derived cells. Hierarchical clustering of the adhesion profiles differentiates metastatic cell lines from primary tumour lines. Furthermore, we uncovered that metastatic cells selectively associate with fibronectin when in combination with galectin-3, galectin-8 or laminin. We show that these molecules correlate with human disease and that their interactions are mediated in part by α3β1 integrin. Thus, our platform allowed us to interrogate interactions between metastatic cells and their microenvironments, and identified extracellular matrix and integrin interactions that could serve as therapeutic targets.

Date: 2012
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DOI: 10.1038/ncomms2128

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