ArticleMolecular biology of the cell2009
Supervillin reorganizes the actin cytoskeleton and increases invadopodial efficiency.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
- KIF14 as a Dual Microtubule/F-Actin Binding Protein Contributing to Cytokinesis.Cytoskeleton (Hoboken, N.J.) · 2026Review
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- G3BP1 reduction during cellular senescence promotes SVIL expression and selected senescence-associated phenotypes.Frontiers in cell and developmental biology · 2026Article
- ORAI1, FGF23, PP13, palladin, and supervillin as potential biomarkers in late-onset pre-eclampsia: a comparative study in maternal and cord blood.BMC pregnancy and childbirth · 2025Article
- Comparative genomic analysis of immune-related genes and chemosensory receptors provides insights into the evolution and adaptation of four major domesticated Asian carps.BMC genomics · 2025Article
- The R-RAS2 GTPase is a signaling hub in triple-negative breast cancer cell metabolism and metastatic behavior.Journal of hematology & oncology · 2025Article
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- Proximity labeling reveals interactions necessary to maintain the distinct apical domains of Drosophila photoreceptors.Journal of cell science · 2024Article
- Cancer cell extravasation requiresBritish journal of cancer · 2024Observational
- Genetic admixture drives climate adaptation in the bank vole.Communications biology · 2024Article
- Using Genomics to Identify Novel Therapeutic Targets for Aortic Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Supervillin Contributes to LPS-induced Inflammatory Response in THP-1 Cell-derived Macrophages.Inflammation · 2022Article
- Proteomic analysis identifies the E3 ubiquitin ligase Pdzrn3 as a regulatory target of Wnt5a-Ror signaling.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Targeting SNARE-Mediated Vesicle Transport to Block Invadopodium-Based Cancer Cell Invasion.Frontiers in oncology · 2021Review
- Supervillin promotes tumor angiogenesis in liver cancer.Oncology reports · 2020Article
- Loss of supervillin causes myopathy with myofibrillar disorganization and autophagic vacuoles.Brain : a journal of neurology · 2020Article
- Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation.BMC genomics · 2019Article
- Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.Journal of experimental & clinical cancer research : CR · 2018Article
- Emerging roles for LPP in metastatic cancer progression.Journal of cell communication and signaling · 2018Review
- Generation and characterization of monoclonal antibodies that recognize human and murine supervillin protein isoforms.PloS one · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Tumor cells use actin-rich protrusions called invadopodia to degrade extracellular matrix (ECM) and invade tissues; related structures, termed podosomes, are sites of dynamic ECM interaction. We show here that supervillin (SV), a peripheral membrane protein that binds F-actin and myosin II, reorganizes the actin cytoskeleton and potentiates invadopodial function. Overexpressed SV induces redistribution of lamellipodial cortactin and lamellipodin/RAPH1/PREL1 away from the cell periphery to internal sites and concomitantly increases the numbers of F-actin punctae. Most punctae are highly dynamic and colocalize with the podosome/invadopodial proteins, cortactin, Tks5, and cdc42. Cortactin binds SV sequences in vitro and contributes to the formation of enhanced green fluorescent protein (EGFP)-SV induced punctae. SV localizes to the cores of Src-generated podosomes in COS-7 cells and with invadopodia in MDA-MB-231 cells. EGFP-SV overexpression increases average numbers of ECM holes per cell; RNA interference-mediated knockdown of SV decreases these numbers. Although SV knockdown alone has no effect, simultaneous down-regulation of SV and the closely related protein gelsolin reduces invasion through ECM. Together, our results show that SV is a component of podosomes and invadopodia and that SV plays a role in invadopodial function, perhaps as a mediator of cortactin localization, activation state, and/or dynamics of metalloproteinases at the ventral cell surface.
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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.