ArticleOncogene2013
Histone deacetylase inhibitors suppress mutant p53 transcription via histone deacetylase 8.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 151 citations in OpenAlex.
- TP53-mutated myelodysplastic syndromes and acute myeloid leukemia: a comprehensive overview of targeted approaches.Frontiers in oncology · 2026Review
- Targeted Degradation of Histone Deacetylase 8 Using Proteolysis Targeting Chimeras Technology: A Promising Approach for Glioblastoma Treatment.Drug design, development and therapy · 2026Article
- Histone Deacetylase Inhibitors orchestrate epigenetic signalling and alter the nucleoporins and nuclear envelope in cervical cancer.Translational oncology · 2025Article
- Maternal Metformin Administration During the Pre-Gestation Period Improves Transient Cerebral Ischemia Injury in Male Offspring Rats.Advanced pharmaceutical bulletin · 2024Article
- Targeting mutant p53: a key player in breast cancer pathogenesis and beyond.Cell communication and signaling : CCS · 2024Review
- P53 together with ferroptosis: a promising strategy leaving cancer cells without escape.Acta biochimica et biophysica Sinica · 2024Article
- HDAC8-mediated inhibition of EP300 drives a transcriptional state that increases melanoma brain metastasis.Nature communications · 2023Article
- Targeting Histone Deacetylases 6 in Dual-Target Therapy of Cancer.Pharmaceutics · 2023Review
- Review
- Bromodomain Protein BRD4-Mediated Mutant p53 Transcription Promotes TNBC Progression.International journal of molecular sciences · 2022Article
- Pathological Role of HDAC8: Cancer and Beyond.Cells · 2022Review
- A Therapeutic Perspective of HDAC8 in Different Diseases: An Overview of Selective Inhibitors.International journal of molecular sciences · 2022Review
- Recent Advances in the Management of Relapsed and Refractory Peripheral T-Cell Lymphomas.Journal of personalized medicine · 2022Review
- Detection and Quantification of Tp53 and p53-Anti-p53 Autoantibody Immune Complex: Promising Biomarkers in Early Stage Lung Cancer Diagnosis.Biosensors · 2022Article
- Homeobox A5 activates p53 pathway to inhibit proliferation and promote apoptosis of adrenocortical carcinoma cells by inducing Aldo-Keto reductase family 1 member B10 expression.Bioengineered · 2021Article
- Crosslink between p53 and metastasis: focus on epithelial-mesenchymal transition, cancer stem cell, angiogenesis, autophagy, and anoikis.Molecular biology reports · 2021Review
- Epigenetic Therapies in Ovarian Cancer Alter Repetitive Element Expression in aCancer research · 2021Article
- Targeting mutant p53 for cancer therapy: direct and indirect strategies.Journal of hematology & oncology · 2021Review
- Network-Based Systems Analysis Explains Sequence-Dependent Synergism of Bortezomib and Vorinostat in Multiple Myeloma.The AAPS journal · 2021Article
- Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mutation of the p53 gene is the most common genetic alteration in human cancer and contributes to malignant process by enhancing transformed properties of cells and resistance to anticancer therapy. Mutant p53 is often highly expressed in tumor cells at least, in part, due to its increased half-life. However, whether mutant p53 expression is regulated by other mechanisms in tumors is unclear. Here we found that histone deacetylase (HDAC) inhibitors suppress both wild-type and mutant p53 transcription in time- and dose-dependent manners. Consistent with this, the levels of wild-type and mutant p53 proteins are decreased upon treatment with HDAC inhibitors. Importantly, we found that upon knockdown of each class I HDAC, only HDAC8 knockdown leads to decreased expression of wild-type and mutant p53 proteins and transcripts. Conversely, we found that ectopic expression of wild-type, but not mutant HDAC8, leads to increased transcription of p53. Furthermore, we found that knockdown of HDAC8 results in reduced expression of HoxA5 and consequently, attenuated ability of HoxA5 to activate p53 transcription, which can be rescued by ectopic expression of HoxA5. Because of the fact that HDAC8 is required for expression of both wild-type and mutant p53, we found that targeted disruption of HDAC8 expression remarkably triggers proliferative defect in cells with a mutant, but not wild-type, p53. Together, our data uncover a regulatory mechanism of mutant p53 transcription via HDAC8 and suggest that HDAC inhibitors and especially HDAC8-targeting agents might be explored as an adjuvant for tumors carrying a mutant p53.
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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.