Extracellular matrix determinants and the regulation of cancer cell invasion stratagems
Open accessAbstract
Summary: During development, wound repair and disease‐related processes, such as cancer, normal, or neoplastic cell types traffic through the extracellular matrix (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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Pepsinized preparations of collagen I lacking the telopeptide cannot be crosslinked, leading to altered dependencies on matrix metalloproteinases (MMPs) for cancer invasion.
“Pepsinized preparations of collagen I lacking the telopeptide cannot be crosslinked, which leads to altered dependencies on matrix metalloproteinases (MMPs) for cancer invasion160.”
From A framework for advancing our understanding of cancer-associated fibroblasts (2020) · cites this paper as [160]
The section on pepsin-extracted collagen hydrogels says pepsin removes crosslink-rich telopeptides and that cancer cells can infiltrate the resulting crosslink-depleted gels without proteases. The section on covalently crosslinked collagen hydrogels reports MMP-dependent invasion in intact gels. The source does not say telopeptide-free collagen cannot be crosslinked at all, or establish loss of crosslinks alone as the cause of the changed MMP dependence; it also discusses pore size. (LLM, conf=0.86)
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Cites
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“Whereas tissue-specific knockouts are seldom employed for these studies, cooperative interactions between cancer cells and stromal cell populations further complicate efforts to identify a single, monolithic player (Gaggioli et al., 2007; Kessenbrock et al., 2010).”
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- Authors
- WILLIS, A. L., SABEH, F., LI, X. ‐., & WEISS, S. J.
- Affiliations
- University of Michigan (US)
- Corresponding author
- WEISS, S.J.
- ORCID
- Venue
- Journal of Microscopy
- Publisher
- Wiley
- Published
- 2013-08-07
- Volume
- 251
- Issue
- 3
- Pages
- 250-260
- ISSN
- 0022-2720 (ISSN-L)
- 1365-2818
- PMC
- PMC6085113
- OpenAlex
- W2136174986
- Cited by
- 85
- References
- 4
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 7 · 2020: 9 · 2019: 4 · 2018: 11 · 2017: 7 · 2016: 11 · 2015: 14 · 2014: 8 · 2013: 2
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Microscopy (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Funders
- NIH (CA88308, CA71699)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- extracellular matrix, tumor invasion, extracellular matrix stiffness, cell motility, tissue structure
- MeSH terms
- Animals, Cell Movement, Extracellular Matrix, Humans, Neoplasms
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