ArticleCurrent biology : CB2014
Vav1 as a central regulator of invadopodia assembly.
Article in Current biology : CB, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
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- PI(3,4,5)P3-mediated Cdc42 activation regulates macrophage podosome assembly.Cellular and molecular life sciences : CMLS · 2025Article
- Ectopic expression of DOCK8 regulates lysosome-mediated pancreatic tumor cell invasion.Cell reports · 2023Article
- Review
- The Cell Biology of Metastatic Invasion in Pancreatic Cancer: Updates and Mechanistic Insights.Cancers · 2023Review
- The scaffold RhoGAP protein ARHGAP8/BPGAP1 synchronizes Rac and Rho signaling to facilitate cell migration.Molecular biology of the cell · 2023Article
- ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia.The Journal of cell biology · 2023Article
- GPCRs thatSmall GTPases · 2022Review
- TC10 regulates breast cancer invasion and metastasis by controlling membrane type-1 matrix metalloproteinase at invadopodia.Communications biology · 2021Article
- Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA).Stem cell reviews and reports · 2021Article
- Actin dynamics during tumor cell dissemination.International review of cell and molecular biology · 2021Review
- The role of actin and myosin in antigen extraction by B lymphocytes.Seminars in cell & developmental biology · 2020Review
- Origin, Organization, Dynamics, and Function of Actin and Actomyosin Networks at the T Cell Immunological Synapse.Annual review of immunology · 2019Review
- TKS5-positive invadopodia-like structures in human tumor surgical specimens.Experimental and molecular pathology · 2019Article
- Identification of Targetable Pathways in Oral Cancer Patients via Random Forest and Chemical Informatics.Cancer informatics · 2019Article
- Rho GTPase signaling complexes in cell migration and invasion.The Journal of cell biology · 2018Review
- Total alkaloids ofOncology letters · 2018Article
- Invading, Leading and Navigating Cells inGenetics · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Invadopodia are protrusive structures used by tumor cells for degradation of the extracellular matrix to promote invasion [1]. Invadopodia formation and function are regulated by cytoskeletal-remodeling pathways and the oncogenic kinase Src. The guanine nucleotide exchange factor Vav1, which is an activator of Rho family GTPases, is ectopically expressed in many pancreatic cancers, where it promotes tumor cell survival and migration [2, 3]. We have now determined that Vav1 is also a potent regulator of matrix degradation by pancreatic tumor cells as depletion of Vav1 by siRNA-mediated knockdown inhibits the formation of invadopodia. This requires the exchange function of Vav1 toward the GTPase Cdc42, which is required for invadopodia assembly [4, 5]. In addition, we have determined that Src-mediated phosphorylation and activation of Vav1 are both required for, and, unexpectedly, sufficient for, invadopodia formation. Expression of Vav1 Y174F, which mimics its activated state, is a potent inducer of invadopodia formation through Cdc42, even in the absence of Src activation and phosphorylation of other Src substrates, such as cortactin. Thus, these data identify a novel mechanism by which Vav1 can enhance the tumorigenicity and invasive potential of cancer cells. These data suggest that Vav1 promotes the matrix-degrading processes underlying tumor cell migration and further, under conditions of ectopic Vav1 expression, that Vav1 is a central regulator and major driver of invasive matrix remodeling by pancreatic tumor cells.
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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.