Rac activation and inactivation control plasticity of tumor cell movement.

By Victoria Sanz‐Moreno, Gilles Gadea, Jessica Ahn, H. Paterson, P. Marra, Sophie E Pinner, Erik Sahai, C. Marshall. Cell, 2008

1,003 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/5f569f1ce215b5ee6081a2c0d3f90258b9655653

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In Cell Biology

1. Valerie M. Weaver
2. Stephanie Alexander
3. J. Mouw
4. A. Ridley
5. Michael W. Pickup
6. M. Schwartz
7. A. Horwitz
8. Peter Friedl

In Molecular Biology

1. Stephanie Alexander
2. A. Ridley
3. Peter Friedl
4. K. Rossman
5. C. Der
6. A. Horwitz
7. J. Parsons
8. J. Mouw

Citations in the corpus

• Cell adhesion: integrating cytoskeletal dynamics and cellular tension (2010, background): “Conversely, Rho can inhibit Rac through a pathway that involves ROCK, possibly through mechanical tension stimulating a Rac GAP such as ARHGAP22 (Ref”
• Tumor heterogeneity: causes and consequences (2009, background): “In this case, the phenotypic differences result from different, mutually exclusive, and inter-convertible activation of Rac and Rho GTPases [23].”
• Rho-Kinase/ROCK: A Key Regulator of the Cytoskeleton and Cell Polarity (2010, background): “Inhibition of Rho-kinase converts their morphology from amoeboid to mesenchymal in a DOCK3 (RacGEF)/Rac/WAVE2-dependent manner, whereas silencing of DOCK3 or Rac1 converts cells from the mesenchymal morphology to amoeboid one in a Rho-kinase/ARHGAP22 (RacGAP)-dependent manner, suggesting that these ”
• Routes and mechanisms of extracellular vesicle uptake (2014, background): “Rac1 is a GTPase which not only has a major role in macropinocytosis (110), but also in regulation of cell growth, cytoskeletal reorganization, protein kinase activation (111) and epithelial-to-mesenchymal transition (EMT) in cancer (112).”
• Rho GTPase signalling in cell migration (2015, background): “For example, cells switch from lamellipodium-driven migration to bleb/ lobopodium-driven migration when RhoA/ROCK activity goes up [49 ,50].”
• The extracellular matrix modulates the hallmarks of cancer (2014, positive): “Thereafter, the nature of the migratory phenotype is dictated by the activity of the dominant Rho-family GTPase; a mesenchymal migratory phenotype is largely dictated by the activity of Rac GTPases while elevated RhoA GTPase activity favors ameboid migration [87].”
• Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited (2009, background): “2 A) (Wolf et al., 2003a,b, 2007; Demou et al., 2005; Carragher et al., 2006; Gadea et al., 2008; Sanz-Moreno et al., 2008).”
• Cancer invasion and the microenvironment: plasticity and reciprocity. (2011, positive): “Alternatively, amoeboid dissemination may originate from collective invasion when cell-cell junctions are abandoned and release the cells toward a single-cell migration program of low integrin-mediated adhesion and high Rho-mediated cortical actomyosin contractility (Hegerfeldt et al., 2002; Sanz-Mo”
• Ras superfamily GEFs and GAPs: validated and tractable targets for cancer therapy? (2010, background): “By contrast, protease-dependent mesenchymal-type movement was driven by DOCK3, a RacGE”