ArticleOncogene2017
Human EHMT2/G9a activates p53 through methylation-independent mechanism.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 55 citations in OpenAlex.
- Discovery of Benzophenanthridine Alkaloids fromPharmaceuticals (Basel, Switzerland) · 2026Article
- EHMT2 aggravates vascular remodeling via epigenetic inhibition of GADD45G.Experimental & molecular medicine · 2026Article
- Chemokines as regulators of CAR-T cell trafficking, function, and context-dependent tumor cell death.Frontiers in immunology · 2026Review
- Glycosylation in cancer: mechanisms, diagnostic markers, and therapeutic applications.Molecular and cellular biochemistry · 2025Review
- EHMT1 mediates cellular motility in embryonal rhabdomyosarcoma by activating SOX8 expression.British journal of cancer · 2025Article
- Modulatory Effect of Curcumin on Expression of Methyltransferase/Demethylase in Colon Cancer Cells: Impact on wt p53, mutp53 and c-Myc.Molecules (Basel, Switzerland) · 2025Article
- EHMT2 as a Candidate Gene for an Autosomal Recessive Neurodevelopmental Syndrome.Molecular neurobiology · 2025Article
- Dualistic role of ZEB1 and ZEB2 in tumor progression.Biology direct · 2025Review
- p53: The Multifaceted Roles of Covalent Modifications in Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes.Journal of translational medicine · 2024Article
- A Review of CAR-T Combination Therapies for Treatment of Gynecological Cancers.International journal of molecular sciences · 2024Review
- Discovery of the First-in-Class G9a/GLP PROTAC Degrader.Journal of medicinal chemistry · 2024Article
- Discovery of the First-in-class G9a/GLP PROTAC Degrader.bioRxiv : the preprint server for biology · 2024Article
- Review
- Experimental Insights into the Interplay between Histone Modifiers and p53 in Regulating Gene Expression.International journal of molecular sciences · 2023Review
- TNFα Effects on Adipocytes Are Influenced by the Presence of Lysine Methyltransferases, G9a (EHMT2) and GLP (EHMT1).Biology · 2023Article
- Article
- Review
- Article
- Opposing Roles of Wild-type and Mutant p53 in the Process of Epithelial to Mesenchymal Transition.Frontiers in molecular biosciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
p53 is a critical tumor suppressor in humans. It functions mostly as a transcriptional factor and its activity is regulated by numerous post-translational modifications. Among different covalent modifications found on p53 the most controversial one is lysine methylation. We found that human G9a (hG9a) unlike its mouse orthologue (mG9a) potently stimulated p53 transcriptional activity. Both ectopic and endogenous hG9a augmented p53-dependent transcription of pro-apoptotic genes, including Bax and Puma, resulting in enhanced apoptosis and reduced colony formation. Significantly, shRNA-mediated knockdown of hG9a attenuated p53-dependent activation of Puma. On the molecular level, hG9a interacted with histone acetyltransferase, p300/CBP, resulting in increased histone acetylation at the promoter of Puma. The bioinformatics data substantiated our findings showing that positive correlation between G9a and p53 expression is associated with better survival of lung cancer patients. Collectively, this study demonstrates that depending on the cellular and organismal context, orthologous proteins may exert both overlapping and opposing functions. Furthermore, this finding has important ramifications on the use of G9a inhibitors in combination with genotoxic drugs to treat p53-positive tumors.
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What OpenQuestion holds
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.