ArticlePigment cell & melanoma research2011
Constitutive Smad linker phosphorylation in melanoma: a mechanism of resistance to transforming growth factor-β-mediated growth inhibition.
Article in Pigment cell & melanoma research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- SMAD2 linker phosphorylation impacts overall survival, proliferation, TGFβ1-dependent gene expression and pluripotency-related proteins in NSCLC.British journal of cancer · 2025Article
- Smad transcription factors as mediators of 7 transmembrane G protein-coupled receptor signalling.Acta pharmacologica Sinica · 2025Review
- Transforming Growth Factor-β/Smad Signaling Inhibits Melanoma Cancer Stem Cell Self-Renewal, Tumor Formation and Metastasis.Cancers · 2024Article
- A novel pathogenic variant located just upstream of the C-terminal Ser423-X-Ser425 phosphorylation motif in SMAD3 causing Loeys-Dietz syndrome.Molecular genetics & genomic medicine · 2023Article
- Smad linker region phosphorylation is a signalling pathway in its own right and not only a modulator of canonical TGF-β signalling.Cellular and molecular life sciences : CMLS · 2020Review
- Phosphorylation status at Smad3 linker region modulates transforming growth factor-β-induced epithelial-mesenchymal transition and cancer progression.Cancer science · 2019Review
- sFRP1 exerts effects on gastric cancer cells through GSK3β/Rac1‑mediated restraint of TGFβ/Smad3 signaling.Oncology reports · 2019Article
- Identification of Epithelial-Mesenchymal Transition-related Target Genes Induced by the Mutation of Smad3 Linker Phosphorylation.Journal of cancer prevention · 2018Article
- Entanglement of GSK-3β, β-catenin and TGF-β1 signaling network to regulate myocardial fibrosis.Journal of molecular and cellular cardiology · 2017Review
- The GSK-3 family as therapeutic target for myocardial diseases.Circulation research · 2015Review
- Definition of smad3 phosphorylation events that affect malignant and metastatic behaviors in breast cancer cells.Cancer research · 2014Article
- Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.Circulation · 2014Article
- TGF-β-activated kinase 1 (Tak1) mediates agonist-induced Smad activation and linker region phosphorylation in embryonic craniofacial neural crest-derived cells.The Journal of biological chemistry · 2013Article
- Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma.Annals of dermatology · 2013Article
- Araf kinase antagonizes Nodal-Smad2 activity in mesendoderm development by directly phosphorylating the Smad2 linker region.Nature communications · 2013Article
- Non-canonical Smads phosphorylation induced by the glutamate release inhibitor, riluzole, through GSK3 activation in melanoma.PloS one · 2012Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Melanoma cells are resistant to transforming growth factor-β (TGFβ)-induced cell-cycle arrest. In this study, we investigated a mechanism of resistance involving a regulatory domain, called linker region, in Smad2 and Smad3, main downstream effectors of TGFβ. Melanoma cells in culture and tumor samples exhibited constitutive Smad2 and Smad3 linker phosphorylation. Treatment of melanoma cells with the MEK1/2 inhibitor, U0126, or the two pan-CDK and GSK3 inhibitors, Flavopiridol and R547, resulted in decreased linker phosphorylation of Smad2 and Smad3. Overexpression of the linker phosphorylation-resistant Smad3 EPSM mutant in melanoma cells resulted in an increase in expression of p15(INK4B) and p21(WAF1) , as compared with cells transfected with wild-type (WT) Smad3. In addition, the cell numbers of EPSM Smad3-expressing melanoma cells were significantly reduced compared with WT Smad3-expressing cells. These results suggest that the linker phosphorylation of Smad3 contributes to the resistance of melanoma cells to TGFβ-mediated growth inhibition.
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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.