ArticleOncogene2004
Activated p53 suppresses the histone methyltransferase EZH2 gene.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 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.
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Who cites it
88 citing papers in PubMed, 193 citations in OpenAlex.
- Expression of EZH2 and Ki-67 in colorectal cancer and associations with treatment response and prognosis.British journal of cancer · 2009Trial
- Epigenetic Targeting of Senescent Cells Prevents the Deleterious Effects of Obstructive Sleep Apnea on Growing Skeleton.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Treating human cancer by targeting EZH2.Genes & diseases · 2025Review
- Targeting EZH2 in Cancer: Mechanisms, Pathways, and Therapeutic Potential.Molecules (Basel, Switzerland) · 2024Review
- Article
- p53 ensures the normal behavior and modification of G1/S-specific histone H3.1 in the nucleus.Life science alliance · 2024Article
- Post-Translational Modifications (PTMs) of mutp53 and Epigenetic Changes Induced by mutp53.Biology · 2024Review
- EZH2 Expression in Head-and-Neck Squamous Cell Cancer in Young Patients.International journal of molecular sciences · 2024Article
- TP53 mutations predict for poor outcomes in patients with newly diagnosed aggressive B-cell lymphomas in the current era.Blood advances · 2023Article
- Downregulation of EZH2 inhibits epithelial-mesenchymal transition in enzalutamide-resistant prostate cancer.The Prostate · 2023Article
- Experimental Insights into the Interplay between Histone Modifiers and p53 in Regulating Gene Expression.International journal of molecular sciences · 2023Review
- Selective nuclear export inhibitor KPT‑330 enhances the radiosensitivity of esophageal carcinoma cells.Experimental and therapeutic medicine · 2023Article
- Critical role of the high mobility group A proteins in hematological malignancies.Hematological oncology · 2022Review
- si-PDGFROxidative medicine and cellular longevity · 2022Article
- Going beyond Polycomb: EZH2 functions in prostate cancer.Oncogene · 2021Review
- Article
- NOTCH and EZH2 collaborate to repress PTEN expression in breast cancer.Communications biology · 2021Article
- Review
- Overexpression of enhance of Zeste homolog 2 (EZH2) in endometrial carcinoma: An NRG Oncology/Gynecologic Oncology Group Study.Gynecologic oncology · 2020Article
- Tat expression led to increased histone 3 tri-methylation at lysine 27 and contributed to HIV latency in astrocytes through regulation of MeCP2 and Ezh2 expression.Journal of neurovirology · 2019Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replicative senescence is an irreversible cell cycle arrest that limits the proliferation of damaged cells and may be an important tumor suppression mechanism in vivo. This process is regulated at critical steps by the tumor suppressor p53. To identify genes that may regulate the senescence process, we performed cDNA microarray analysis of gene expression in senescent, young proliferating, and hTERT-immortalized primary human fibroblasts. The histone methyltransferase (HMTase), EZH2, was specifically downregulated in senescent cells. Activated p53 suppressed EZH2 gene expression through repression of the EZH2 gene promoter. This activity of p53 requires intact p53 transactivation and DNA binding domains. Furthermore, the repression of EZH2 promoter by p53 is dependent on p53 transcriptional target p21(Waf1) inactivating RB/E2F pathways. In addition, the knockdown of EZH2 expression retards cell proliferation and induces G2/M arrest. We suggest that the p53-dependent suppression of EZH2 expression is a novel pathway that contributes to p53-mediated G2/M arrest. EZH2 associated complex possesses HMTase activity and is involved in epigenetic regulation. Activated p53 suppresses EZH2 expression, suggesting a further role for p53 in epigenetic regulation and in the maintenance of genetic stability. Suppression of EZH2 expression in tumors by p53 may lead to novel approaches to control cancer progression.
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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.