ArticleOncogene2003
p53-independent induction of Gadd45 by histone deacetylase inhibitor: coordinate regulation by transcription factors Oct-1 and NF-Y.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 131 citations in OpenAlex.
- HDAC inhibitors modulate Hippo pathway signaling in hormone positive breast cancer.Clinical epigenetics · 2025Article
- Exploring CDKN1A Upregulation Mechanisms: Insights into Cell Cycle Arrest Induced by NC2603 Curcumin Analog in MCF-7 Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Role of Histone Deacetylase 6 and Histone Deacetylase 6 Inhibition in Colorectal Cancer.Pharmaceutics · 2023Review
- Nuclear complement C3b promotes paclitaxel resistance by assembling the SIN3A/HDAC1/2 complex in non-small cell lung cancer.Cell death & disease · 2023Article
- High expression of transcription factor POU2F1 confers improved survival on smokers with lung adenocarcinoma: a retrospective study of two cohorts.Translational lung cancer research · 2023Article
- Non-Hydroxamate Zinc-Binding Groups as Warheads for Histone Deacetylases.Molecules (Basel, Switzerland) · 2021Review
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- Tau Stabilizes Chromatin Compaction.Frontiers in cell and developmental biology · 2021Article
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- Apoptosis Induction byHistone Deacetylase Inhibitors in Cancer Cells: Role of Ku70.International journal of molecular sciences · 2019Review
- Combinatorial screening using orthotopic patient derived xenograft-expanded early phase cultures of osteosarcoma identify novel therapeutic drug combinations.Cancer letters · 2019Article
- GADD45α-targeted suicide gene therapy driven by synthetic CArG promoter E9NS sensitizes NSCLC cells to cisplatin, resveratrol, and radiation regardless of p53 status.OncoTargets and therapy · 2019Article
- DNA damage response induced by Etoposide promotes steroidogenesis via GADD45A in cultured adrenal cells.Scientific reports · 2018Article
- GADD45A and CDKN1A are involved in apoptosis and cell cycle modulatory effects of viscumTT with further inactivation of the STAT3 pathway.Scientific reports · 2018Article
- Article
- Long noncoding RNAOncotarget · 2017Article
- Molecular-targeting therapies against quantitative abnormalities in gene expression with malignant tumors.Cancer science · 2017Review
- Article
- The Oct1 transcription factor and epithelial malignancies: Old protein learns new tricks.Biochimica et biophysica acta · 2016Review
- DNA-damage response gene GADD45A induces differentiation in hematopoietic stem cells without inhibiting cell cycle or survival.Stem cells (Dayton, Ohio) · 2016Article
4 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
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase (HDAC) inhibitors cause growth arrest at the G1 and/or G2/M phases, and induce differentiation and/or apoptosis in a wide variety of tumour cells. The growth arrest at G1 phase by HDAC inhibitors is thought to be highly dependent on the upregulation of p21/WAF1, but the precise mechanism by which HDAC inhibitors cause G2/M arrest or apoptosis in tumour cells is unknown. Gadd45 causes cell cycle arrest at the G2/M phase transition and participates in genotoxic stress-induced apoptosis. We show here that it is also induced by a typical HDAC inhibitor, trichostatin A (TSA), through its promoter, in a p53-independent manner. To identify the mechanism of activation of the gadd45 promoter, we performed luciferase reporter analyses and electrophoretic mobility shift assays. These revealed that both the Oct-1 and CCAAT sites are needed for the full activation by TSA. We also found that the transcription factors Oct-1 and NF-Y specifically bind to each site. Thus, HDAC inhibitors can induce Gadd45 through its promoter without the need for functional p53, and both the Oct-1 and NF-Y concertedly participate in TSA-induced activation of the gadd45 promoter.
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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.