ArticleOncogene2017
HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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The trial behind it
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Who cites it
62 citing papers in PubMed, 104 citations in OpenAlex.
- p53-mediated epigenetic regulation in the pathogenesis of endometriosis.Epigenetics · 2026Review
- A FoxM1/Smad4 positive feedback loop promotes pancreatic cancer progression.Cell death & disease · 2026Article
- HDAC1 Regulates Acquired Resistance to EGFR Inhibitors through the TFCP2-NDRG1 Signaling Axis in Pancreatic Cancer.International journal of biological sciences · 2026Article
- Endothelial mechanosensitive transcription factor BHLHE40 induced by Piezo1 suppresses endothelial ferroptosis and inflammation via SLC7A11.Cell death discovery · 2025Article
- Histone Deacetylase Inhibitors orchestrate epigenetic signalling and alter the nucleoporins and nuclear envelope in cervical cancer.Translational oncology · 2025Article
- Advances in pancreatic cancer epigenetics: From the mechanism to the clinic.World journal of gastrointestinal oncology · 2025Review
- Histone deacetylases 10 as a prognostic biomarker correlates with tumor microenvironment and therapy response in colorectal cancer.World journal of gastroenterology · 2025Article
- Review
- CircCFL1 Promotes TNBC Stemness and Immunoescape via Deacetylation-Mediated c-Myc Deubiquitylation to Facilitate Mutant TP53 Transcription.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- HDAC2 promotes autophagy-associated HCC malignant progression by transcriptionally activating LAPTM4B.Cell death & disease · 2024Article
- Post-Translational Modifications (PTMs) of mutp53 and Epigenetic Changes Induced by mutp53.Biology · 2024Review
- Characterization of a novel HDAC2 pathogenetic variant: a missing puzzle piece for chromatinopathies.Human genetics · 2024Article
- Histone deacetylases maintain expression of the pluripotent gene network via recruitment of RNA polymerase II to coding and noncoding loci.Genome research · 2024Article
- Update on histone deacetylase inhibitors in peripheral T-cell lymphoma (PTCL).Clinical epigenetics · 2023Review
- Targeted therapy using nanocomposite delivery systems in cancer treatment: highlighting miR34a regulation for clinical applications.Cancer cell international · 2023Review
- HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023Review
- Exploiting the molecular subtypes and genetic landscape in pancreatic cancer: the quest to find effective drugs.Frontiers in genetics · 2023Review
- Protein acylation: mechanisms, biological functions and therapeutic targets.Signal transduction and targeted therapy · 2022Review
- Targeting the MYC interaction network in B-cell lymphoma via histone deacetylase 6 inhibition.Oncogene · 2022Article
- Porcine Deltacoronavirus Infection Cleaves HDAC2 to Attenuate Its Antiviral Activity.Journal of virology · 2022Article
2 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
18 authors at 9 institutions in 2 countries.
Funding
Abstract
Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We further show that HDAC1, HDAC2 and MYC directly bind to the TP53 gene and that MYC recruitment drops upon HDAC inhibitor treatment. Therefore, our results illustrate a previously unrecognized class I HDAC-dependent control of the TP53 gene and provide evidence for a contribution of MYC. A combined approach targeting HDAC1/HDAC2 and MYC may present a novel and molecularly defined strategy to target mutant p53 in pancreatic cancer.
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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.