ReviewCancer science2019
Phosphorylation status at Smad3 linker region modulates transforming growth factor-β-induced epithelial-mesenchymal transition and cancer progression.
Review in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- The Activation Status of the TGF-β Transducer Smad2 Is Associated with a Reduced Survival in Gastrointestinal Cancers: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2019Pooled it
- Reprogramming in delipidated adipocytes: metabolism, regulation and progress.Cell death discovery · 2026Review
- Rabeprazole attenuates fibrosis by modulating SMAD3 linker region phosphorylation.Biomedical reports · 2026Article
- Ivermectin inhibits ER, HER2, and TGF-β pathways in ER-positive and endocrine-resistant breast cancer cells.PloS one · 2026Article
- Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells.Molecular oncology · 2025Article
- Smad transcription factors as mediators of 7 transmembrane G protein-coupled receptor signalling.Acta pharmacologica Sinica · 2025Review
- A positive feedback loop between SMAD3 and PINK1 in regulation of mitophagy.Cell discovery · 2025Article
- Roles of Post-Translational Modifications of Transcription Factors Involved in Breast Cancer Hypoxia.Molecules (Basel, Switzerland) · 2025Review
- Identification of a Potent CDK8 Inhibitor Using Structure-Based Virtual Screening.Journal of chemical information and modeling · 2025Article
- Oxymatrine inhibited the progression of renal cell carcinoma by increasing TOR1AIP1 expression.Frontiers in pharmacology · 2025Article
- NSUN5 Facilitates Hepatocellular Carcinoma Progression by Increasing SMAD3 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Acetylation-regulated DUSP1 deficiency contributes to renal fibrosis progression.Theranostics · 2025Article
- Endothelial CD38-induced endothelial-to-mesenchymal transition is a pivotal driver in pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2024Article
- Bio-Pathological Functions of Posttranslational Modifications of Histological Biomarkers in Breast Cancer.Molecules (Basel, Switzerland) · 2024Review
- Article
- Hepatitis B virus X protein and TGF-β: partners in the carcinogenic journey of hepatocellular carcinoma.Frontiers in oncology · 2024Review
- Jagged1 intracellular domain/SMAD3 complex transcriptionally regulates TWIST1 to drive glioma invasion.Cell death & disease · 2023Article
- Article
- Beneficial Effects of a Curcumin Derivative and Transforming Growth Factor-β Receptor I Inhibitor Combination on Nonalcoholic Steatohepatitis.Diabetes & metabolism journal · 2023Article
- Integration of Chemoinformatics and Multi-Omics Analysis Defines ECT2 as a Potential Target for Cancer Drug Therapy.Biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Smad3, a major transcription factor in transforming growth factor-β (TGF-β) signaling, plays critical roles in both tumor-suppressive and pro-oncogenic functions. Upon TGF-β stimulation, the C-terminal tail of Smad3 undergoes phosphorylation that is essential for canonical TGF-β signaling. The Smad3 linker region contains serine/threonine phosphorylation sites and can be phosphorylated by intracellular kinases, such as the MAPK family, cyclin-dependent kinase (CDK) family and glycogen synthase kinase-3β (GSK-3β). Previous reports based on cell culture studies by us and others showed that mutation of Smad3 linker phosphorylation sites dramatically intensifies TGF-β responses as well as growth-inhibitory function and epithelial-mesenchymal transition (EMT), suggesting that Smad3 linker phosphorylation suppresses TGF-β transcriptional activities. However, recent discoveries of Smad3-interacting molecules that preferentially bind phosphorylated Smad3 linker serine/threonine residues have shown a multitude of signal transductions that either enhance or suppress TGF-β responses associated with Smad3 turnover or cancer progression. This review aims at providing new insight into the perplexing mechanisms of TGF-β signaling affected by Smad3 linker phosphorylation and further attempts to gain insight into elimination and protection of TGF-β-mediated oncogenic and growth-suppressive signals, respectively.
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What OpenQuestion holds
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.