ArticleEpigenetics2014
SETD6 controls the expression of estrogen-responsive genes and proliferation of breast carcinoma cells.
Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 42 citations in OpenAlex.
- Histone Deacetylase Inhibitors orchestrate epigenetic signalling and alter the nucleoporins and nuclear envelope in cervical cancer.Translational oncology · 2025Article
- SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells.NAR cancer · 2025Article
- RAD18 methylation by the methyltransferase SETD6 attenuates DNA breaks.Scientific reports · 2025Article
- Orchestrating epigenetics: a comprehensive review of the methyltransferase SETD6.Experimental & molecular medicine · 2025Review
- Advances in targeting histone deacetylase for treatment of solid tumors.Journal of hematology & oncology · 2024Review
- Investigating the functional role of SETD6 in lung adenocarcinoma.BMC cancer · 2023Article
- BRD4 methylation by the methyltransferase SETD6 regulates selective transcription to control mRNA translation.Science advances · 2021Article
- Arginine and lysine methylation of MRPS23 promotes breast cancer metastasis through regulating OXPHOS.Oncogene · 2021Article
- Silencing of SETD6 inhibits the tumorigenesis of oral squamous cell carcinoma by inhibiting methylation of PAK4 and RelA.Histology and histopathology · 2021Article
- SET domain containing protein 5 (SETD5) enhances tumor cell invasion and is associated with a poor prognosis in non-small cell lung cancer patients.BMC cancer · 2019Article
- Genome-Wide CRISPR Screen Reveals Autophagy Disruption as the Convergence Mechanism That Regulates the NRF2 Transcription Factor.Molecular and cellular biology · 2019Article
- The methyltransferase SETD6 regulates Mitotic progression through PLK1 methylation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Screening for long noncoding RNAs associated with oral squamous cell carcinoma reveals the potentially oncogenic actions of DLEU1.Cell death & disease · 2018Article
- Human ex vivo prostate tissue model system identifies ING3 as an oncoprotein.British journal of cancer · 2018Article
- Review
- Article
- Regulation of Epigenetic Modifiers, Including KDM6B, by Interferon-γ and Interleukin-4 in Human Macrophages.Frontiers in immunology · 2017Article
- Dysregulation of histone methyltransferases in breast cancer - Opportunities for new targeted therapies?Molecular oncology · 2016Review
- Mechanism of Histone H3K4me3 Recognition by the Plant Homeodomain of Inhibitor of Growth 3.The Journal of biological chemistry · 2016Article
- PAK4 Methylation by SETD6 Promotes the Activation of the Wnt/β-Catenin Pathway.The Journal of biological chemistry · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The lysine methyltransferase SETD6 modifies the histone variant H2AZ, a key component of nuclear receptor-dependent transcription. Herein, we report the identification of several factors that associate with SETD6 and are implicated in nuclear hormone receptor signaling. Specifically, SETD6 associates with the estrogen receptor α (ERα), histone deacetylase HDAC1, metastasis protein MTA2, and the transcriptional co-activator TRRAP. Luciferase reporter assays identify SETD6 as a transcriptional repressor, in agreement with its association with HDAC1 and MTA2. However, SETD6 behaves as a co-activator of several estrogen-responsive genes, such as PGR and TFF1. Consistent with these results, silencing of SETD6 in several breast carcinoma cell lines induced cellular proliferation defects accompanied by enhanced expression of the cell cycle inhibitor CDKN1A and induction of apoptosis. Herein, we have identified several chromatin proteins that associate with SETD6 and described SETD6 as an essential factor for nuclear receptor signaling and cellular proliferation.
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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.