ArticleThe Journal of biological chemistry2016
Rapid Remodeling of Invadosomes by Gi-coupled Receptors: DISSECTING THE ROLE OF Rho GTPases.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Novel pleiotropic risk loci for melanoma and nevus density implicate multiple biological pathways.Nature communications · 2018Pooled it
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- Ischemic accumulation of succinate induces Cdc42 succinylation and inhibits neural stem cell proliferation after cerebral ischemia/reperfusion.Neural regeneration research · 2023Article
- ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia.The Journal of cell biology · 2023Article
- A type IV Autotaxin inhibitor ameliorates acute liver injury and nonalcoholic steatohepatitis.EMBO molecular medicine · 2022Article
- Identification of guanine nucleotide exchange factors that increase Cdc42 activity in primary human endothelial cells.Small GTPases · 2021Article
- YAP and endothelin-1 signaling: an emerging alliance in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Imaging of Genetically Encoded FRET-Based Biosensors to Detect GPCR Activity.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Advances in Understanding TKS4 and TKS5: Molecular Scaffolds Regulating Cellular Processes from Podosome and Invadopodium Formation to Differentiation and Tissue Homeostasis.International journal of molecular sciences · 2020Review
- Tumor Cellular and Microenvironmental Cues Controlling Invadopodia Formation.Frontiers in cell and developmental biology · 2020Review
- Nck adapter proteins promote podosome biogenesis facilitating extracellular matrix degradation and cancer invasion.Cancer medicine · 2019Article
- Profilin binding couples chloride intracellular channel protein CLIC4 to RhoA-mDia2 signaling and filopodium formation.The Journal of biological chemistry · 2018Article
- Endothelin-1 receptor drives invadopodia: Exploiting how β-arrestin-1 guides the way.Small GTPases · 2018Review
- S100A4 regulates macrophage invasion by distinct myosin-dependent and myosin-independent mechanisms.Molecular biology of the cell · 2018Article
- Characterization of Genetically Encoded FRET Biosensors for Rho-Family GTPases.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Nck deficiency is associated with delayed breast carcinoma progression and reduced metastasis.Molecular biology of the cell · 2017Article
- The balance between GαMolecular biology of the cell · 2017Article
- A CDC42-centered signaling unit is a dominant positive regulator of endothelial integrity.Scientific reports · 2017Article
- Flat clathrin lattices are dynamic actin-controlled hubs for clathrin-mediated endocytosis and signalling of specific receptors.Nature communications · 2017Article
- Optogenetic activation of Plexin-B1 reveals contact repulsion between osteoclasts and osteoblasts.Nature communications · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Invadosomes are actin-rich membrane protrusions that degrade the extracellular matrix to drive tumor cell invasion. Key players in invadosome formation are c-Src and Rho family GTPases. Invadosomes can reassemble into circular rosette-like superstructures, but the underlying signaling mechanisms remain obscure. Here we show that Src-induced invadosomes in human melanoma cells (A375M and MDA-MB-435) undergo rapid remodeling into dynamic extracellular matrix-degrading rosettes by distinct G protein-coupled receptor agonists, notably lysophosphatidic acid (LPA; acting through the LPA1 receptor) and endothelin. Agonist-induced rosette formation is blocked by pertussis toxin, dependent on PI3K activity and accompanied by localized production of phosphatidylinositol 3,4,5-trisphosphate, whereas MAPK and Ca(2+) signaling are dispensable. Using FRET-based biosensors, we show that LPA and endothelin transiently activate Cdc42 through Gi, concurrent with a biphasic decrease in Rac activity and differential effects on RhoA. Cdc42 activity is essential for rosette formation, whereas G12/13-mediated RhoA-ROCK signaling suppresses the remodeling process. Our results reveal a Gi-mediated Cdc42 signaling axis by which G protein-coupled receptors trigger invadosome remodeling, the degree of which is dictated by the Cdc42-RhoA activity balance.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.