Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited

By F. Sabeh, R. Shimizu-Hirota, S. Weiss. Journal of Cell Biology, 2009

660 citations recorded by the source corpus.

Tissue invasion during metastasis requires cancer cells to negotiate a stromal environment dominated by cross-linked networks of type I collagen. Although cancer cells are known to use proteinases to sever collagen networks and thus ease their passage through these barriers, migration across extracellular matrices has also been reported to occur by protease-independent mechanisms, whereby cells squeeze through collagen-lined pores by adopting an ameboid phenotype. We investigate these alternate models of motility here and demonstrate that cancer cells have an absolute requirement for the membrane-anchored metalloproteinase MT1-MMP for invasion, and that protease-independent mechanisms of cell migration are only plausible when the collagen network is devoid of the covalent cross-links that characterize normal tissues.

Subfields: Cancer Research, Cell Biology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/204a91b7eabb92b487f214545b0f34ea9d1cb9f0

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Citations in the corpus

Hallmarks of cancer: the next generation. (2011, neutral): “Less clear is the prevalence of an ‘‘amoeboid’’ form of invasion (Madsen and Sahai, 2010; Sabeh et al., 2009), in which individual cancer cells show morphological plasticity, enabling them to slither through existing interstices in the extracellular matrix rather than clearing a path for themselves,”
Dynamic interplay between the collagen scaffold and tumor evolution (2010, background): “Thus, collagen degradation by proteases, including cathepsins and MMPs, and uptake of the degraded collagen is important for cancer cell invasion [10,45, 46].”
Collagen-based cell migration models in vitro and in vivo. (2009, background): “Fibrils then eceive slow secondary modification by stromal cell-derived lysyl xidase (LOX) which generates aldehyde groups at telopeptideocated lysyl or hydroxylysyl-residues that then spontaneously orm aldimide (Schiff-base) cross-links with amino groups from neighbouring collagen monomer [1,2].”
Matrix Metalloproteinases: Regulators of the Tumor Microenvironment (2010, background): “It remains a subject of ongoing debate whether the amoeboid migration mode is only relevant under in vitro conditions when the surrounding collagen network is devoid of covalent crosslinks (Sabeh et al., 2009).”
DAMPs, PAMPs, and LAMPs in Immunity and Sterile Inflammation. (2020, background): “Proteolytic cleavage has been postulated to be the mechanism by which leukocytes breach this formidable barrier, similar to cancer cell invasion (52).”
Collagen-Based Biomaterials for Tissue Engineering Applications (2010, background): “In this way, the invasive character of cancer cells [113,114] and interaction between cancer cells and other cell types in a 3D environment can be analysed [115].”
Leukocyte migration into inflamed tissues. (2014, background): “Proteolytic cleavage of BM constituents by emigrating leukocytes has long been considered as a possible mechanism, because it has been implicated in cancer cell invasiveness and intravasation (Sabeh et al., 2009).”