ArticleMolecular and cellular biology2018
Depletion of Mediator Kinase Module Subunits Represses Superenhancer-Associated Genes in Colon Cancer Cells.
Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Implication of the Mediator kinase module in CIZ1 recruitment and gene silencing byEpigenetics reports · 2025Article
- Med13 and Med13L: Critical redundant players in basal cardiac function and gene expression.Journal of molecular and cellular cardiology plus · 2025Article
- The MicroRNA miR-454 and the mediator complex component MED12 are regulators of the androgen receptor pathway in prostate cancer.Scientific reports · 2025Article
- The Prognostic Significance of TRs in Hepatocellular Carcinoma: Insights from TCGA and GEO Databases.Biomarker insights · 2025Article
- Bromodomain-containing 4 as a therapeutic target in inflammatory bowel diseases and colorectal cancer.Frontiers in pharmacology · 2025Review
- Subunits Med12 and Med13 of Mediator Cooperate with Subunits SAYP and Bap170 of SWI/SNF in Active Transcription inInternational journal of molecular sciences · 2024Article
- MED12 and CDK8/19 Modulate Androgen Receptor Activity and Enzalutamide Response in Prostate Cancer.Endocrinology · 2024Article
- Targeting super-enhancer activity for colorectal cancer therapy.American journal of translational research · 2024Review
- Clinical Correlates of Venetoclax-Based Combination Sensitivities to Augment Acute Myeloid Leukemia Therapy.Blood cancer discovery · 2023Article
- Super-enhancers complexes zoom in transcription in cancer.Journal of experimental & clinical cancer research : CR · 2023Review
- Review
- The Mediator kinase module: an interface between cell signaling and transcription.Trends in biochemical sciences · 2022Review
- Genome-wide screens identify specific drivers of mutantProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The emerging role of mediator complex subunit 12 in tumorigenesis and response to chemotherapeutics.Cancer · 2020Review
- MED13L integrates Mediator-regulated epigenetic control into lung cancer radiosensitivity.Theranostics · 2020Article
- Targeting transcriptional machinery to inhibit enhancer-driven gene expression in heart failure.Heart failure reviews · 2019Review
- Regulatory functions of the Mediator kinases CDK8 and CDK19.Transcription · 2019Review
- Regulation of cardiac transcription by thyroid hormone and Med13.Journal of molecular and cellular cardiology · 2019Article
- Super-Enhancers in the Regulation of Gene Transcription: General Aspects and Antitumor Targets.Acta naturaeArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cancer, oncogene activation is partly mediated by acquired superenhancers, which therefore represent potential targets for inhibition. Superenhancers are enriched for BRD4 and Mediator, and both BRD4 and the Mediator MED12 subunit are disproportionally required for expression of superenhancer-associated genes in stem cells. Here we show that depletion of Mediator kinase module subunit MED12 or MED13 together with MED13L can be used to reduce expression of cancer-acquired superenhancer genes, such as the MYC gene, in colon cancer cells, with a concomitant decrease in proliferation. Whereas depletion of MED12 or MED13/MED13L caused a disproportional decrease of superenhancer gene expression, this was not seen with depletion of the kinases cyclin-dependent kinase 9 (CDK8) and CDK19. MED12-MED13/MED13L-dependent superenhancer genes were coregulated by β-catenin, which has previously been shown to associate with MED12. Importantly, β-catenin depletion caused reduced binding of MED12 at the MYC superenhancer. The effect of MED12 or MED13/MED13L depletion on cancer-acquired superenhancer gene expression was more specific than and partially distinct from that of BRD4 depletion, with the most efficient inhibition seen with combined targeting. These results identify a requirement of MED12 and MED13/MED13L for expression of acquired superenhancer genes in colon cancer, implicating these Mediator subunits as potential therapeutic targets for colon cancer, alone or together with BRD4.
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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.