ArticlePloS one2013
ß1 integrin binding phosphorylates ezrin at T567 to activate a lipid raft signalsome driving invadopodia activity and invasion.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- The unphosphorylated, closed form of ezrin binds to RNA to maintain a metastatic phenotype in osteosarcoma cells.Science signaling · 2026Article
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- Ezrin defines TSC complex activation at endosomal compartments through EGFR-AKT signaling.eLife · 2025Article
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- Effects of periodic mechanical stress on cytoskeleton dependent lipid raft-induced integrin ɑ1 activation in rat nucleus pulposus cells.Journal of molecular histology · 2023Article
- Cotranslational interaction of human EBP50 and ezrin overcomes masked binding site during complex assembly.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Integrin-Linked Kinase Links Integrin Activation to Invadopodia Function and Invasion via the p(T567)-Ezrin/NHERF1/NHE1 Pathway.International journal of molecular sciences · 2021Article
- Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review.Frontiers in cell and developmental biology · 2020Review
- Tumor Cellular and Microenvironmental Cues Controlling Invadopodia Formation.Frontiers in cell and developmental biology · 2020Review
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- Inhibition of ezrin causes PKCα-mediated internalization of erbb2/HER2 tyrosine kinase in breast cancer cells.The Journal of biological chemistry · 2019Article
- Urokinase-type plasminogen activator (uPA) promotes ezrin-mediated reorganization of the synaptic cytoskeleton in the ischemic brain.The Journal of biological chemistry · 2018Article
- NHE1 has a notable role in metastasis and drug resistance of T-cell acute lymphoblastic leukemia.Oncology letters · 2017Article
- Transient mechanical strain promotes the maturation of invadopodia and enhances cancer cell invasionJournal of cell science · 2017Article
- Regulation of invadopodia by mechanical signaling.Experimental cell research · 2016Review
- Matrix rigidity differentially regulates invadopodia activity through ROCK1 and ROCK2.Biomaterials · 2016Article
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- Podoplanin mediates ECM degradation by squamous carcinoma cells through control of invadopodia stability.Oncogene · 2015Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular matrix (ECM) degradation is a critical process in tumor cell invasion and requires matrix degrading protrusions called invadopodia. The Na(+)/H(+) exchanger (NHE1) has recently been shown to be fundamental in the regulation of invadopodia actin cytoskeleton dynamics and activity. However, the structural link between the invadopodia cytoskeleton and NHE1 is still unknown. A candidate could be ezrin, a linker between the NHE1 and the actin cytoskeleton known to play a pivotal role in invasion and metastasis. However, the mechanistic basis for its role remains unknown. Here, we demonstrate that ezrin phosphorylated at T567 is highly overexpressed in the membrane of human breast tumors and positively associated with invasive growth and HER2 overexpression. Further, in the metastatic cell line, MDA-MB-231, p-ezrin was almost exclusively expressed in invadopodia lipid rafts where it co-localized in a functional complex with NHE1, EGFR, ß1-integrin and phosphorylated-NHERF1. Manipulation by mutation of ezrins T567 phosphorylation state and/or PIP2 binding capacity or of NHE1s binding to ezrin or PIP2 demonstrated that p-ezrin expression and binding to PIP2 are required for invadopodia-mediated ECM degradation and invasion and identified NHE1 as the membrane protein that p-ezrin regulates to induce invadopodia formation and activity.
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Registered trials
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.