ArticlePloS one2013
Activation of p21 by HDAC inhibitors requires acetylation of H2A.Z.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Epigenetic regulation of breast cancer metastasis.Cancer metastasis reviews · 2024Review
- CDKN1A/p21 in Breast Cancer: Part of the Problem, or Part of the Solution?International journal of molecular sciences · 2023Review
- Recent advancement of HDAC inhibitors against breast cancer.Medical oncology (Northwood, London, England) · 2023Review
- Dual LSD1 and HDAC6 Inhibition Induces Doxorubicin Sensitivity in Acute Myeloid Leukemia Cells.Cancers · 2022Article
- A novel SNF2 ATPase complex in Trypanosoma brucei with a role in H2A.Z-mediated chromatin remodelling.PLoS pathogens · 2022Article
- HDAC Inhibitors for the Therapy of Triple Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway.Biology open · 2021Article
- Article
- Article
- A three layered histone epigenetics in breast cancer metastasis.Cell & bioscience · 2020Review
- Article
- Epigenetic Regulation of p21Cancers · 2019Review
- The histone variant H2A.Z in gene regulation.Epigenetics & chromatin · 2019Review
- Article
- Review
- Effects of Histone Deacetylase Inhibitor Panobinostat (LBH589) on Bone Marrow Mononuclear Cells of Relapsed or Refractory Multiple Myeloma Patients and Its Mechanisms.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- The pro-apoptotic BAX protein influences cell growth and differentiation from the nucleus in healthy interphasic cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Article
- CUDC-101, a Novel Inhibitor of Full-Length Androgen Receptor (flAR) and Androgen Receptor Variant 7 (AR-V7) Activity: Mechanism of Action and In Vivo Efficacy.Hormones & cancer · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differential positioning of the histone variant H2A.Z in a p53 dependent manner was shown to regulate p21 transcription. Whether H2A.Z is involved in p21 activity in the absence of p53 is not known. The p21 gene is repressed in estrogen receptor (ER) negative cell lines that are p53-/- and hormone independent for their growth. Here we demonstrate that class I and II pan Histone deacetylase inhibitors (HDACi) induce p21 transcription and reduce cell proliferation of MDA-MB231, an ERα-negative mammary tumor cell line, in a H2A.Z dependent manner. H2A.Z is associated with the transcription start site (TSS) of the repressed p21 gene. Depleting H2A.Z did not lead to transcription of p21 but annihilated the stimulating effect of HDACi on this gene. Acetylation of H2A.Z but not of H3K9 at the p21 promoter correlated with p21 activation. We further show that HDACi treatment reduced the presence of the p400 chromatin remodeler at the p21 TSS. We propose a model in which association of p400 negatively affects p21 transcription by interfering with acetylation of H2A.Z.
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