ArticleMolecular and cellular biology2003
Histone deacetylation of RB-responsive promoters: requisite for specific gene repression but dispensable for cell cycle inhibition.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 78 citations in OpenAlex.
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- Emerging therapeutic strategies in cancer therapy by HDAC inhibition as the chemotherapeutic potent and epigenetic regulator.Medical oncology (Northwood, London, England) · 2024Review
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.bioRxiv : the preprint server for biology · 2023Article
- Rb-E2F-HDAC Repressor Complexes Control Interferon-Induced Repression of Adenovirus To Promote Persistent Infection.Journal of virology · 2022Article
- Intravitreal HDAC Inhibitor Belinostat Effectively Eradicates Vitreous Seeds Without Retinal Toxicity In Vivo in a Rabbit Retinoblastoma Model.Investigative ophthalmology & visual science · 2021Article
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- Role of Nitric Oxide in Gene Expression Regulation during Cancer: Epigenetic Modifications and Non-Coding RNAs.International journal of molecular sciences · 2021Review
- 8a, a New Acridine Antiproliferative and Pro-Apoptotic Agent Targeting HDAC1/DNMT1.International journal of molecular sciences · 2021Article
- Synergistic Enhancement of Cancer Therapy Using HDAC Inhibitors: Opportunity for Clinical Trials.Frontiers in genetics · 2020Review
- Effects of β-carotene on Expression of Selected MicroRNAs, Histone Acetylation, and DNA Methylation in Colon Cancer Stem Cells.Journal of cancer prevention · 2019Article
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- Nutrient-driven O-GlcNAc cycling - think globally but act locally.Journal of cell science · 2014Article
- Targeting histone deacetylases for cancer therapy: from molecular mechanisms to clinical implications.International journal of biological sciences · 2014Review
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- PTTG1 attenuates drug-induced cellular senescence.PloS one · 2011Article
- One function--multiple mechanisms: the manifold activities of p53 as a transcriptional repressor.Journal of biomedicine & biotechnology · 2011Review
- [Signal transduction in urothelial cancer: how exactly do we know the targets for targeted therapy?].Der Urologe. Ausg. A · 2010Article
- p65 Negatively regulates transcription of the cyclin E gene.The Journal of biological chemistry · 2010Article
- Drosophila RB proteins repress differentiation-specific genes via two different mechanisms.Molecular and cellular biology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The retinoblastoma tumor suppressor protein (RB) is targeted for inactivation in the majority of human tumors, underscoring its critical role in attenuating cellular proliferation. RB inhibits proliferation by repressing the transcription of genes that are essential for cell cycle progression. To repress transcription, RB assembles multiprotein complexes containing chromatin-modifying enzymes, including histone deacetylases (HDACs). However, the extent to which HDACs participate in transcriptional repression and are required for RB-mediated repression has not been established. Here, we investigated the role of HDACs in RB-dependent cell cycle inhibition and transcriptional repression. We find that active RB mediates histone deacetylation on cyclin A, Cdc2, topoisomerase IIalpha, and thymidylate synthase promoters. We also demonstrate that this deacetylation is HDAC dependent, since the HDAC inhibitor trichostatin A (TSA) prevented histone deacetylation at each promoter. However, TSA treatment blocked RB repression of only a specific subset of genes, thereby demonstrating that the requirement of HDACs for RB-mediated transcriptional repression is promoter specific. The HDAC-independent repression was not associated with DNA methylation or gene silencing but was readily reversible. We show that this form of repression resulted in altered chromatin structure and was dependent on SWI/SNF chromatin remodeling activity. Importantly, we find that cell cycle inhibitory action of RB is not intrinsically dependent on the ability to recruit HDAC activity. Thus, while HDACs do play a major role in RB-mediated repression, they are dispensable for the repression of critical targets leading to cell cycle arrest.
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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.