The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
A combinatorial extracellular matrix platform identifies cell-extracellular matrix interactions that correlate with metastasis
Open accessAbstract
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. Interactions of cells with extracellular matrix are important in normal physiology and cancer metastasis. Here, an extracellular matrix molecule array is developed and used to show that conserved changes in adhesive properties are associated with metastasis, including binding to fibronectin in combination with galectin-3, galectin-8 or laminin.
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Cites
Gene expression profiling predicts clinical outcome of breast cancer
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Microenvironmental regulation of metastasis
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The Extracellular Matrix: Not Just Pretty Fibrils
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Self-citationGene-expression profiles predict survival of patients with lung adenocarcinoma
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Carcinoma-associated fibroblasts stimulate tumor progression of initiated human epithelium
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Self-citationBreast cancer cells produce tenascin C as a metastatic niche component to colonize the lungs
Oskarsson, T., Acharyya, S., Zhang, X. H.-F., Vanharanta, S., Tavazoie, S. F., Morris, P. G., Downey, R. J., Manova-Todorova, K., Brogi, E., & Massagué, J. (2011) · Nature Medicine · doi:10.1038/nm.2379 · Cited by 869
Suppression of lung adenocarcinoma progression by Nkx2-1
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Cited by
Remodelling the extracellular matrix in development and disease
Bonnans, C., Chou, J., & Werb, Z. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3904 · Cited by 4,367
Metastatic Stem Cells: Sources, Niches, and Vital Pathways
Oskarsson, T., Batlle, E., & Massagué, J. (2014) · Cell Stem Cell · doi:10.1016/j.stem.2014.02.002 · Cited by 708
Integrins and cancer: regulators of cancer stemness, metastasis, and drug resistance
Seguin, L., Desgrosellier, J. S., Weis, S. M., & Cheresh, D. A. (2015) · Trends in Cell Biology · doi:10.1016/j.tcb.2014.12.006 · Cited by 685
Fibrous nonlinear elasticity enables positive mechanical feedback between cells and ECMs
Hall, M. S., Alisafaei, F., Ban, E., Feng, X., Hui, C.-Y., Shenoy, V. B., & Wu, M. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1613058113 · Cited by 360
Meiners, S., Eickelberg, O., & Königshoff, M. (2015) · European Respiratory Journal · doi:10.1183/09031936.00186914 · Cited by 340
Metadata
- Authors
- Reticker-Flynn, N. E., Malta, D. F. B., Winslow, M. M., Lamar, J. M., Xu, M. J., Underhill, G. H., Hynes, R. O., Jacks, T. E., & Bhatia, S. N.
- Venue
- Nature Communications
- Published
- 2012-10-09
- Volume
- 3
- Issue
- 1
- Pages
- 1122-1122
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W1874945197
- Cited by
- 195
- References
- 12
- FWCI
- 11.25
- Type
- journal article
- Language
- en
- Open access
- bronze
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