Differing modes of tumour cell invasion have distinct requirements for Rho/ROCK signalling and extracellular proteolysis

By Erik Sahai, C. Marshall. Nature Cell Biology, 2003

1,226 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/87c7420be2aaebc603f3a29981b00d4ca7524971

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Citations in the corpus

The role of focal-adhesion kinase in cancer — a new therapeutic opportunity (2005, background): “Interestingly, it is now recognized that tumour cells can invade a 3D matrix by both MMP-dependent and MMP-independent mechanisms — referred to as mesenchymal-like and amoeboid-like mechanisms, respectivel”
MicroRNAs — the micro steering wheel of tumour metastases (2009, background): “RHOA signalling through kinases ROCK1 (Rho-associated, coiled-coil-containing protein kinase 1) and ROCK2 is central to producing the actomyosin contractile forces required for the mesenchymal–amoeboid transitio”
Mitf regulation of Dia1 controls melanoma proliferation and invasiveness. (2006, background): “…cells Rho–ROCK signaling is required for a form of invasion of three-dimensional matrices that is characterised by a membrane-blebbing morphology (Sahai and Marshall 2003; Wilkinson et al. 2005), more akin to an amoeboid form of cell invasion than the mesenchymal elongated form of migration…”
Actin dynamics, architecture, and mechanics in cell motility. (2014, background): “Furthermore, enhanced contractility of both invading cancer cells and the fibroblasts that accompany them has been linked to more aggressive cancers (94, 269, 272).”
Chemotaxis in cancer (2011, background): “In tumour cells, responses to changes in the microenvironment can induce rapid transitions between these modes of migratio”
Illuminating the metastatic process (2007, background): “, and this plasticity can enable them to continue moving even when one type of motility has been prevented by pharmacological mean”
Tumor cell traffic through the extracellular matrix is controlled by the membrane-anchored collagenase MT1-MMP (2004, background): “Similarly, nonproteolytic systems have been reported to confer tumor cells with the ability to traverse Matrigel-coated surfaces (Hotary et al., 2000; Sahai and Marshall, 2003), a noncross-linked composite of basement membrane-associated macromolecules (Kleinman et al.”
The role of disturbed pH dynamics and the Na+/H+ exchanger in metastasis (2005, background): “Conditions that increase invasive capacity often provoke a dramatic shift in cell morphology from AMOEBOID MORPHOTYPE to MESENCHYMAL MORPHOTYPE , which corresponds with the increase in invasive capacit”
Cancer invasion and the microenvironment: plasticity and reciprocity. (2011, neutral): “Mesenchymal invasion may undergo secondary conversion to amoeboid, rounded migration by diverse mechanisms, such as a decrease in Rac activity and concomitant activation of Rho-mediated actomyosin contractility (Sahai and Marshall, 2003).”
CDK inhibitors: cell cycle regulators and beyond. (2008, neutral): “For instance, cells that migrate with an elongated morphology require Rac activity, whereas cells migrating with a rounded morphology depend on Rho/ ROCK signals (Sahai and Marshall, 2003).”
Rho-Kinase/ROCK: A Key Regulator of the Cytoskeleton and Cell Polarity (2010, background): “However, the question of whether these two Rho-kinase proteins are qualitatively different or expressed at different abundances in tissues remains unanswered.”
Multi-step pericellular proteolysis controls the transition from individual to collective cancer cell invasion (2007, background): “Conversely, in high-density non-fibrillar ECM including reconstituted basement membrane lacking discrete gaps, the abrogation of proteolytic activity impairs cell migration more stringentl”
The physics of cancer: the role of physical interactions and mechanical forces in metastasis (2011, neutral): “By contrast, inhibition of the master mediators of actomyosin contractility, ROCK and RHO, forces the adoption of a mesenchymal migration mode in cells with an intrinsic amoeboid shape when embedded in Matrige”