ArticleCell death & disease2013
Incompatible effects of p53 and HDAC inhibition on p21 expression and cell cycle progression.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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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
24 citing papers in PubMed, 39 citations in OpenAlex.
- Dalpiciclib plus chidamide in HR + /HER2-advanced breast cancer after CDK4/6 inhibitor failure: a phase Ib trial.Nature communications · 2026Article
- Reversing Bladder Cancer Chemo-resistance through Blocking Cell Senescence by a Combination Therapy.Theranostics · 2026Article
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Plasma oncology: Adjuvant therapy for head and neck cancer using cold atmospheric plasma.Frontiers in oncology · 2022Review
- Chidamide combined with paclitaxel effectively reverses the expression of histone deacetylase in lung cancer.Anti-cancer drugs · 2020Article
- Riluzole Enhances the Response of Human Nasopharyngeal Carcinoma Cells to Ionizing Radiation via ATM/P53 Signalling Pathway.Journal of Cancer · 2020Article
- Small molecule activators of the p53 response.Journal of molecular cell biology · 2019Review
- Article
- Targeting negative regulation of p53 by MDM2 and WIP1 as a therapeutic strategy in cutaneous melanoma.British journal of cancer · 2018Article
- Gold-chrysophanol nanoparticles suppress human prostate cancer progression through inactivating AKT expression and inducing apoptosis and ROS generation in vitro and in vivo.International journal of oncology · 2017Article
- Integrated analysis of the molecular action of Vorinostat identifies epi-sensitised targets for combination therapy.Oncotarget · 2017Article
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- CDKN1A histone acetylation and gene expression relationship in gastric adenocarcinomas.Clinical and experimental medicine · 2017Article
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- Histone deacetylase inhibitor screening identifies HC toxin as the most effective in intrahepatic cholangiocarcinoma cells.Oncology reports · 2016Article
- Targeting HDAC with a novel inhibitor effectively reverses paclitaxel resistance in non-small cell lung cancer via multiple mechanisms.Cell death & disease · 2016Article
- Lentivirus-mediated Knockdown of HDAC1 Uncovers Its Role in Esophageal Cancer Metastasis and Chemosensitivity.Journal of Cancer · 2016Article
- HDAC and HDAC Inhibitor: From Cancer to Cardiovascular Diseases.Chonnam medical journal · 2016Review
- Knockdown of Rad9A enhanced DNA damage induced by trichostatin A in esophageal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Mdm2 inhibition confers protection of p53-proficient cells from the cytotoxic effects of Wee1 inhibitors.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Nutlin-3 selectively activates p53 by inhibiting the interaction of this tumor suppressor with its negative regulator murine double minute 2 (mdm2), while trichostatin A (TSA) is one of the most potent histone deacetylase (HDAC) inhibitors currently available. As both Nutlin-3 and TSA increase the levels of the cell cycle inhibitor p21(cip1/waf1) in cells, we investigated whether a combination of these compounds would further augment p21 levels. Contrary to expectations, we found that short-term exposure to Nutlin-3 and TSA in combination did not have an additive effect on p21 expression. Instead, we observed that activation of p53 prevented the ability of TSA to increase p21 levels. Furthermore, TSA inhibited Nutlin-3-induced expression of p53-dependent mRNAs including P21. This negative effect of TSA on Nutlin-3 was significantly less pronounced in the case of hdm2, another p53 downstream target. Aside from suggesting a model to explain these incompatible effects of Nutlin-3 and TSA, we discuss the implications of our findings in cancer therapy and cell reprogramming.
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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.