ArticleCancers2021
Inhibiting FAK-Paxillin Interaction Reduces Migration and Invadopodia-Mediated Matrix Degradation in Metastatic Melanoma Cells.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Single-cell lineage tracing maps clonal and transcriptional dynamics in melanoma metastasis.bioRxiv : the preprint server for biology · 2026Article
- Attenuated lamin A-prohibitin2 interaction leads to mitochondrial dysfunction in LMNA 289 A>G-mediated dilated cardiomyopathy.The Journal of biological chemistry · 2026Article
- Establishing selectivity of FAK-paxillin PPI inhibitor using pulldown proteomics and a focal adhesion protein selectivity panel.Biochemistry and biophysics reports · 2026Article
- Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026Review
- Melanoma: Pathogenesis and Targeted Therapy.MedComm · 2026Review
- Article
- Phenotype switching in highly invasive resistant to vemurafenib and cobimetinib melanoma cells.Cell communication and signaling : CCS · 2025Article
- Conformational dynamics and multimodal interaction of Paxillin with the focal adhesion targeting domain.Science advances · 2025Article
- Conformational dynamics and multi-modal interaction of Paxillin with the Focal Adhesion Targeting Domain.bioRxiv : the preprint server for biology · 2025Article
- Structure-based discovery of hydrocarbon-stapled paxillin peptides that block FAK scaffolding in cancer.Nature communications · 2025Article
- Paxillin and Kindlin: Research Progress and Biological Functions.Biomolecules · 2025Review
- Paxillin promotes the invasion and migration of polyploid giant cancer cells with daughter cells after arsenic trioxide treatment by regulating the expression of cathepsin B/D.Journal of Cancer · 2025Article
- Focal adhesion kinase signaling - tumor vulnerabilities and clinical opportunities.Journal of cell science · 2024Review
- Cell-Material Interplay in Focal Adhesion Points.ACS applied materials & interfaces · 2024Article
- Adhesion, metastasis, and inhibition of cancer cells: a comprehensive review.Molecular biology reports · 2024Review
- Progerin Inhibits the Proliferation and Migration of Melanoma Cells by Regulating the Expression of Paxillin.OncoTargets and therapy · 2024Article
- The Role of Paxillin Aberrant Expression in Cancer and Its Potential as a Target for Cancer Therapy.International journal of molecular sciences · 2023Review
- Protein dynamics at invadopodia control invasion-migration transitions in melanoma cells.Cell death & disease · 2023Article
- Glioblastoma multiforme: Diagnosis, treatment, and invasion.Journal of biomedical research · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nonreceptor tyrosine kinase FAK is a promising target for solid tumor treatment because it promotes invasion, tumor progression, and drug resistance when overexpressed. Investigating the role of FAK in human melanoma cells, we found that both in situ and metastatic melanoma cells strongly express FAK, where it controls tumor cells' invasiveness by regulating focal adhesion-mediated cell motility. Inhibiting FAK in human metastatic melanoma cells with either siRNA or a small inhibitor targeting the kinase domain impaired migration but led to increased invadopodia formation and extracellular matrix degradation. Using FAK mutated at Y397, we found that this unexpected increase in invadopodia activity is due to the lack of phosphorylation at this residue. To preserve FAK-Src interaction while inhibiting pro-migratory functions of FAK, we found that altering FAK-paxillin interaction, with either FAK mutation in the focal adhesion targeting (FAT) domain or a competitive inhibitor peptide mimicking paxillin LD domains drastically reduces cell migration and matrix degradation by preserving FAK activity in the cytoplasm. In conclusion, our data show that targeting FAK-paxillin interactions could be a potential therapeutic strategy to prevent metastasis formation, and molecules targeting this interface could be alternative to inhibitors of FAK kinase activity which display unexpected effects.
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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 Socratic graph.