ArticleThe Journal of cell biology2012
Hic-5 promotes invadopodia formation and invasion during TGF-β-induced epithelial-mesenchymal transition.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 154 citations in OpenAlex.
- RASAL2 activates RAC1 to promote triple-negative breast cancer progression.The Journal of clinical investigation · 2014Trial
- P95-HER2 promotes metastatic progression by biasing MRTFA dependent signaling.bioRxiv : the preprint server for biology · 2026Article
- EMT and cell cycle control invadopodia and metastasis in breast cancer via Filip1L.Research square · 2026Article
- Hic-5 drives epithelial mechanotransduction promoting a feed-forward cycle of bronchoconstriction.Nature communications · 2025Article
- Invadopodia in cancer metastasis: dynamics, regulation, and targeted therapies.Journal of translational medicine · 2025Review
- Key LncRNAs Associated with Distant Metastasis in Breast Cancer: A System Biology Analysis.MicroRNA (Shariqah, United Arab Emirates) · 2025Article
- A comparative analysis of paxillin and Hic-5 proximity interactomes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Constructing a doxycycline-inducible system for an epithelial-to-mesenchymal transition model in MCF10A cells.Biology open · 2024Article
- POTEE promotes breast cancer cell malignancy by inducing invadopodia formation through the activation of SUMOylated Rac1.Molecular oncology · 2024Article
- Hic-5 regulates extracellular matrix-associated gene expression and cytokine secretion in cancer associated fibroblasts.Experimental cell research · 2024Article
- FilGAP, a GAP for Rac1, down-regulates invadopodia formation in breast cancer cells.Cell structure and function · 2023Article
- Isotoosendanin exerts inhibition on triple-negative breast cancer through abrogating TGF-Acta pharmaceutica Sinica. B · 2023Article
- SYK-mediated epithelial cell state is associated with response to c-Met inhibitors in c-Met-overexpressing lung cancer.Signal transduction and targeted therapy · 2023Article
- Suppressing of Src-Hic-5-JNK-AKT Signaling Reduced GAPDH Expression for Preventing the Progression of HuCCT1 Cholangiocarcinoma.Pharmaceutics · 2022Article
- Proteolytic and mechanical remodeling of the extracellular matrix by invadopodia in cancer.Physical biology · 2022Review
- A proliferative to invasive switch is mediated by srGAP1 downregulation through the activation of TGF-β2 signaling.Cell reports · 2022Article
- Invadopodia enable cooperative invasion and metastasis of breast cancer cells.Communications biology · 2022Article
- Targeting Src-Hic-5 Signal Cascade for Preventing Migration of Cholangiocarcinoma Cell HuCCT1.Biomedicines · 2022Article
- Jagged-1 is induced by mTOR inhibitors in renal cancer cells through an Akt/ALK5/Smad4-dependent mechanism.Current research in pharmacology and drug discovery · 2022Article
- Discoidin Domain Receptor 1, a Potential Biomarker and Therapeutic Target in Hepatocellular Carcinoma.International journal of general medicine · 2022Review
37 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor β (TGF-β)-stimulated epithelial-mesenchymal transition (EMT) is an important developmental process that has also been implicated in increased cell invasion and metastatic potential of cancer cells. Expression of the focal adhesion protein Hic-5 has been shown to be up-regulated in epithelial cells in response to TGF-β. Herein, we demonstrate that TGF-β-induced Hic-5 up-regulation or ectopic expression of Hic-5 in normal MCF10A cells promoted increased extracellular matrix degradation and invasion through the formation of invadopodia. Hic-5 was tyrosine phosphorylated in an Src-dependent manner after TGF-β stimulation, and inhibition of Src activity or overexpression of a Y38/60F nonphosphorylatable mutant of Hic-5 inhibited matrix degradation and invasion. RhoC, but not RhoA, was also required for TGF-β- and Hic-5-induced matrix degradation. Hic-5 also induced matrix degradation, cell migration, and invasion in the absence of TGF-β via Rac1 regulation of p38 MAPK. These data identify Hic-5 as a critical mediator of TGF-β-stimulated invadopodia formation, cell migration, and invasion.
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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.