ArticleOncotarget2014
Histone deacetylase 2 and N-Myc reduce p53 protein phosphorylation at serine 46 by repressing gene transcription of tumor protein 53-induced nuclear protein 1.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Anticancer Effects of I-BET151, an Inhibitor of Bromodomain and Extra-Terminal Domain Proteins.Frontiers in oncology · 2021Review
- JMJD6 is a tumorigenic factor and therapeutic target in neuroblastoma.Nature communications · 2019Article
- Review: Precision medicine and driver mutations: Computational methods, functional assays and conformational principles for interpreting cancer drivers.PLoS computational biology · 2019Review
- PRIMA-1Journal of experimental & clinical cancer research : CR · 2019Article
- Epigenetic regulation of neuroblastoma development.Cell and tissue research · 2018Review
- Targeting of epigenetic regulators in neuroblastoma.Experimental & molecular medicine · 2018Review
- Minichromosome maintenance protein 2 and 3 promote osteosarcoma progression via DHX9 and predict poor patient prognosis.Oncotarget · 2017Article
- Pharmacological targeting of BET proteins inhibits renal fibroblast activation and alleviates renal fibrosis.Oncotarget · 2016Article
- p73 promotes glioblastoma cell invasion by directly activating POSTN (periostin) expression.Oncotarget · 2016Article
- The role of HDAC2 in chromatin remodelling and response to chemotherapy in ovarian cancer.Oncotarget · 2016Article
- HDAC2 deregulation in tumorigenesis is causally connected to repression of immune modulation and defense escape.Oncotarget · 2015Article
- Up-regulation of HDAC9 promotes cell proliferation through suppressing p53 transcription in osteosarcoma.International journal of clinical and experimental medicine · 2015Article
- The structural basis for cancer treatment decisions.Oncotarget · 2014Review
- Histone deacetylase 6 activity is critical for the metastasis of Burkitt's lymphoma cells.Cancer cell international · 2014Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 4 countries.
Funding
Abstract
Myc oncoproteins and histone deacetylases (HDACs) exert oncogenic effects by modulating gene transcription. Paradoxically, N-Myc induces p53 gene expression. Tumor protein 53-induced nuclear protein 1 (TP53INP1) phosphorylates p53 protein at serine 46, leading to enhanced p53 activity, transcriptional activation of p53 target genes and programmed cell death. Here we aimed to identify the mechanism through which N-Myc overexpressing p53 wild-type neuroblastoma cells acquired resistance to apoptosis. TP53INP1 was found to be one of the genes most significantly repressed by HDAC2 and N-Myc according to Affymetrix microarray gene expression datasets. HDAC2 and N-Myc reduced TP53INP1 gene expression by direct binding to the TP53INP1 gene promoter, leading to transcriptional repression of TP53INP1, p53 protein de-phosphorylation at serine 46, neuroblastoma cell proliferation and survival. Moreover, low levels of TP53INP1 expression in human neuroblastoma tissues correlated with high levels of N-Myc expression and poor patient outcome, and the BET bromodomain inhibitors JQ1 and I-BET151 reduced N-Myc expression and reactivated TP53INP1 expression in neuroblastoma cells. These findings identify TP53INP1 repression as an important co-factor for N-Myc oncogenesis, and provide further evidence for the potential application of BET bromodomain inhibitors in the therapy of N-Myc-induced neuroblastoma.
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