ArticleNucleic acids research2012
Estrogen receptor-α recruits P-TEFb to overcome transcriptional pausing in intron 1 of the MYB gene.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Aspirin might reduce the incidence of breast cancer: An updated meta-analysis of 38 observational studies.Medicine · 2020Pooled it
- Single-molecule live imaging of subunit interactions and exchange within cellular regulatory complexes.Molecular cell · 2025Article
- CDK9 inhibitors for the treatment of solid tumors.Biochemical pharmacology · 2024Review
- An enhancer RNA recruits KMT2A to regulate transcription of Myb.Cell reports · 2024Article
- c-myb is involved in CML progression and is a therapeutic target in the zebrafish CML model.Animal models and experimental medicine · 2024Article
- Targeting CDK9 with selective inhibitors or degraders in tumor therapy: an overview of recent developments.Cancer biology & therapy · 2023Review
- An enhancer RNA recruits MLL1 to regulate transcription ofbioRxiv : the preprint server for biology · 2023Article
- Synthetic oleanane triterpenoids suppressFrontiers in oncology · 2023Article
- Antitumoral Activity of a CDK9 PROTAC Compound in HER2-Positive Breast Cancer.International journal of molecular sciences · 2022Article
- Destabilization of macrophage migration inhibitory factor by 4-IPP reduces NF-κB/P-TEFb complex-mediated c-Myb transcription to suppress osteosarcoma tumourigenesis.Clinical and translational medicine · 2022Article
- RNA polymerase II pausing in development: orchestrating transcription.Open biology · 2022Review
- Review
- c-Myb interferes with inflammatory IL1α-NF-κB pathway in breast cancer cells.Neoplasia (New York, N.Y.) · 2021Article
- CDK9: A Comprehensive Review of Its Biology, and Its Role as a Potential Target for Anti-Cancer Agents.Frontiers in oncology · 2021Review
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Targeting transcription factors in cancer drug discovery.Exploration of targeted anti-tumor therapy · 2020Review
- The mechanism of MYB transcriptional regulation by MLL-AF9 oncoprotein.Scientific reports · 2019Article
- Article
- Transcription regulation ofAnnals of translational medicine · 2018Review
- Reassessing the Potential of Myb-targeted Anti-cancer Therapy.Journal of Cancer · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MYB proto-oncogene is expressed in most estrogen receptor-positive (ERα(+)) breast tumors and cell lines. Expression of MYB is controlled, in breast cancer and other cell types, by a transcriptional pausing mechanism involving an attenuation site located ∼1.7 kb downstream from the transcription start site. In breast cancer cells, ligand-bound ERα binds close to, and drives transcription beyond this attenuation site, allowing synthesis of complete transcripts. However, little is known, in general, about the factors involved in relieving transcriptional attenuation, or specifically how ERα coordinates such factors to promote transcriptional elongation. Using cyclin dependent kinase 9 (CDK9) inhibitors, reporter gene assays and measurements of total and intronic MYB transcription, we show that functionally active CDK9 is required for estrogen-dependent transcriptional elongation. We further show by ChIP and co-immunoprecipitation studies that the P-TEFb complex (CDK9/CyclinT1) is recruited to the attenuation region by ligand-bound ERα, resulting in increased RNA polymerase II Ser-2 phosphorylation. These data provide new insights into MYB regulation, and given the critical roles of MYB in tumorigenesis, suggest targeting MYB elongation as potential therapeutic strategy.
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