Rho-GTPase signaling drives melanoma cell plasticity.
To investigate mechanisms that underlie different modes of tumor cell movement we have studied how regulation of the activity of the Rho family GTPases determines the mode of tumor cell movement. Guanine nucleotide exchange factors (GEFs) and GTPase accelerating proteins (GAPs) are key regulators of the activity of small GTPases with GEFs promoting activation to the GTP bound state and GAPs promoting inactivation by stimulating GTP hydrolysis. We identified two important signaling pathways regulating amoeboid and mesenchymal types of motility in melanoma. Here, we discuss our findings in the context of how specificity of Rho signaling is achieved by GEFs and GAPs.
Sanz-Moreno
Victoria
V
Institute of Cancer Research, Cancer Research UK Centre for Cell and Molecular Biology, London, UK.
Marshall
Christopher J
CJ
D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D006801:Humans; D008545:Melanoma / Q000201:enzymology* / Q000473:pathology*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010750:Phosphoproteins / Q000378:metabolism; D015398:Signal Transduction; D051300:Wiskott-Aldrich Syndrome Protein Family / Q000378:metabolism; D020742:rhoA GTP-Binding Protein / Q000378:metabolism*
D048868:Adaptor Proteins, Signal Transducing; D009419:Nerve Tissue Proteins; D010750:Phosphoproteins; D051300:Wiskott-Aldrich Syndrome Protein Family; D020742:rhoA GTP-Binding Protein