Journal
JOURNAL OF MICROSCOPY
Volume 251, Issue 3, Pages 250-260Publisher
WILEY
DOI: 10.1111/jmi.12064
Keywords
Extracellular matrix (ECM); invasion; MT1-MMP
Categories
Funding
- NIH [CA88308, CA71699]
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During development, wound repair and disease-related processes, such as cancer, normal, or neoplastic cell types traffic through the extracellularmatrix (ECM), the complex composite of collagens, elastin, glycoproteins, proteoglycans, and glycosaminoglycans that dictate tissue architecture. Current evidence suggests that tissue-invasive processes may proceed by protease-dependent or protease-independent strategies whose selection is not only governed by the characteristics of the motile cell population, but also by the structural properties of the intervening ECM. Herein, we review the mechanisms by which ECM dimensionality, elasticity, crosslinking, and pore size impact patterns of cell invasion. This summary should prove useful when designing new experimental approaches for interrogating invasion programs as well as identifying potential cellular targets for next-generation therapeutics.
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