ArticleOncogene2007
p300 is required for orderly G1/S transition in human cancer cells.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 57 citations in OpenAlex.
- Exploring the therapeutic role of carnosol in cancer: from molecular insights to clinical promise.Medical oncology (Northwood, London, England) · 2025Review
- Ubiquitin proteasome system (UPS): a crucial determinant of the epigenetic landscape in cancer.Epigenomics · 2025Review
- Targeting Triple-Negative Breast Cancer by the Phytopolyphenol Carnosol: ROS-Dependent Mechanisms.Antioxidants (Basel, Switzerland) · 2023Review
- Crosstalk of the Wnt/β-Catenin Signaling Pathway in the Induction of Apoptosis on Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The Biological Significance of Targeting Acetylation-Mediated Gene Regulation for Designing New Mechanistic Tools and Potential Therapeutics.Biomolecules · 2021Review
- Protein acetylation and deacetylation: An important regulatory modification in gene transcription (Review).Experimental and therapeutic medicine · 2020Review
- Hypothesis: Retinoblastoma protein inactivation mediates effects of histone deacetylase inhibitor-induced Wnt hyperactivation in colorectal cancer cells.Journal of Cancer · 2020Article
- Gcn5-mediated acetylation at MBF-regulated promoters induces the G1/S transcriptional wave.Nucleic acids research · 2019Article
- Inhibitor of CBP Histone Acetyltransferase Downregulates p53 Activation and Facilitates Methylation at Lysine 27 on Histone H3.Molecules (Basel, Switzerland) · 2018Article
- Opposing roles of the aldo-keto reductases AKR1B1 and AKR1B10 in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- Exploitation of EP300 and CREBBP Lysine Acetyltransferases by Cancer.Cold Spring Harbor perspectives in medicine · 2017Review
- Inhibition of bromodomain and extra-terminal (BET) proteins increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of cMYC-IRF4-miR-125b interplay.Journal of hematology & oncology · 2016Article
- Salicylate, diflunisal and their metabolites inhibit CBP/p300 and exhibit anticancer activity.eLife · 2016Article
- Negative regulation of the p300-p53 interplay by DDX24.Oncogene · 2016Article
- Protein lysine acetylation by p300/CBP.Chemical reviews · 2015Review
- Histone acetyltransferase inhibitor II induces apoptosis in glioma cell lines via the p53 signaling pathway.Journal of experimental & clinical cancer research : CR · 2014Article
- Overexpression of histone deacetylases in cancer cells is controlled by interplay of transcription factors and epigenetic modulators.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Prepaying the entropic cost for allosteric regulation in KIX.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Structure of the p300 histone acetyltransferase bound to acetyl-coenzyme A and its analogues.Biochemistry · 2014Article
- Regulation of histone modifying enzymes by the ubiquitin-proteasome system.Biochimica et biophysica acta · 2014Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the transcriptional coactivator p300 in cell cycle control has not been analysed in detail due to the lack of appropriate experimental systems. We have now examined cell cycle progression of p300-deficient cancer cell lines, where p300 was disrupted either by gene targeting (p300(-) cells) or knocked down using RNAi. Despite significant proliferation defects under normal growth conditions, p300-deficient cells progressed rapidly through G1 with premature S-phase entry. Accelerated G1/S transition was associated with early retinoblastoma (RB) hyperphosphorylation and activation of E2F targets. The p300-acetylase activity was dispensable since expression of a HAT-deficient p300 mutant reversed these changes. Co-immunoprecipitation showed p300/RB interaction occurs in vivo during G1, and this interaction has two peaks: in early G1 with unphosphorylated RB and in late G1 with phosphorylated RB. In vitro kinase assays showed that p300 directly inhibits cdk6-mediated RB phosphorylation, suggesting p300 acts in early G1 to prevent RB hyperphosphorylation and delay premature S-phase entry. Paradoxically, continued cycling of p300(-) cells despite prolonged serum depletion was observed, and this occurred in association with persistent RB hyperphosphorylation. Altogether, these results suggest that p300 has an important role in G1/S control, possibly by modulating RB phosphorylation.
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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.