ArticleCells2021
EB1 Restricts Breast Cancer Cell Invadopodia Formation and Matrix Proteolysis via FAK.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- Comprehensive molecular characterization of high-stemness gastric cancer cells using single-cell transcriptomics, spatial mapping, and machine learning.NPJ precision oncology · 2025Article
- A structured framework of cytoskeletal proteins and noncentrosomal microtubules promotes the initiation and elongation of invadopodia.Molecular biology of the cell · 2025Article
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- Oncogenic mechanisms of COL10A1 in cancer and clinical challenges (Review).Oncology reports · 2024Review
- Tumor invasiveness is regulated by the concerted function of APC, formins, and Arp2/3 complex.iScience · 2024Article
- CLIP170 inhibits the metastasis and EMT of papillary thyroid cancer through the TGF-β pathway.Medical oncology (Northwood, London, England) · 2024Article
- Inhibition of histone deacetylase 6 destabilizes ERK phosphorylation and suppresses cancer proliferation via modulation of the tubulin acetylation-GRP78 interaction.Journal of biomedical science · 2023Article
- Targeting SNARE-Mediated Vesicle Transport to Block Invadopodium-Based Cancer Cell Invasion.Frontiers in oncology · 2021Review
- Cell surface engineering for inhibition of breast cancer cell motility through modulation of mechanotransduction and focal adhesion dynamics.Journal of tissue engineeringArticle
- Adenomatous Polyposis Coli (APC) in cell migration.European journal of cell biologyReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulation of microtubule dynamics by plus-end tracking proteins (+TIPs) plays an essential role in cancer cell migration. However, the role of +TIPs in cancer cell invasion has been poorly addressed. Invadopodia, actin-rich protrusions specialized in extracellular matrix degradation, are essential for cancer cell invasion and metastasis, the leading cause of death in breast cancer. We, therefore, investigated the role of the End Binding protein, EB1, a major hub of the +TIP network, in invadopodia functions. EB1 silencing increased matrix degradation by breast cancer cells. This was recapitulated by depletion of two additional +TIPs and EB1 partners, APC and ACF7, but not by the knockdown of other +TIPs, such as CLASP1/2 or CLIP170. The knockdown of Focal Adhesion Kinase (FAK) was previously proposed to similarly promote invadopodia formation as a consequence of a switch of the Src kinase from focal adhesions to invadopodia. Interestingly, EB1-, APC-, or ACF7-depleted cells had decreased expression/activation of FAK. Remarkably, overexpression of wild type FAK, but not of FAK mutated to prevent Src recruitment, prevented the increased degradative activity induced by EB1 depletion. Overall, we propose that EB1 restricts invadopodia formation through the control of FAK and, consequently, the spatial regulation of Src activity.
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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.