ArticleEMBO reports2018
Smad3-mediated recruitment of the methyltransferase SETDB1/ESET controls
Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 68 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- Methylome profiling of SetDB1-deficient ESCs reveals coordinated epigenetic cross-talk during pluripotency.Stem cell reports · 2026Article
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- ZNF274 constrains lineage plasticity and drives intrinsic resistance to CDK7 inhibitors in pancreatic cancer.Nature communications · 2026Article
- The epigenetic regulator SETDB1 as a key component of cancer stem cells and drug resistance in primary liver cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Review
- Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.The Kaohsiung journal of medical sciences · 2025Review
- [Epithelial-mesenchymal Transition: Biological Basis and Clinical Prospects of Lung Cancer Invasion, Metastasis, and Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy.Current cancer drug targets · 2025Review
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- SETDB1 modulates the TGFβ response in Duchenne muscular dystrophy myotubes.Science advances · 2024Article
- Genetic analysis of PALB2 gene WD40 domain in canine mammary tumour patients.Veterinary medicine and science · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Harnessing function of EMT in cancer drug resistance: a metastasis regulator determines chemotherapy response.Cancer metastasis reviews · 2024Review
- Targeting SMAD-Dependent Signaling: Considerations in Epithelial and Mesenchymal Solid Tumors.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Pancreatic Neuroendocrine Tumors: Signaling Pathways and Epigenetic Regulation.International journal of molecular sciences · 2024Review
- The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease.Epigenetics & chromatin · 2023Review
- Cancer metastasis under the magnifying glass of epigenetics and epitranscriptomics.Cancer metastasis reviews · 2023Review
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- From shape-shifting embryonic cells to oncology: The fascinating history of epithelial mesenchymal transition.Seminars in cancer biology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
During epithelial-mesenchymal transition (EMT), reprogramming of gene expression is accompanied by histone modifications. Whether EMT-promoting signaling directs functional changes in histone methylation has not been established. We show here that the histone lysine methyltransferase SETDB1 represses EMT and that, during TGF-β-induced EMT, cells attenuate SETDB1 expression to relieve this inhibition. SETDB1 also controls stem cell generation, cancer cell motility, invasion, metastatic dissemination, as well as sensitivity to certain cancer drugs. These functions may explain the correlation of breast cancer patient survival with
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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.