ArticleOncogene2011
Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
The trial behind it
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
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- Exosome-Mediated Lectin Pathway and Resistin-MIF-AA Metabolism Axis Drive Immune Dysfunction in Immune Thrombocytopenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- IER5 Negatively Regulates Cdc25B Expression in HeLa Cells After Gamma Ray Irradiation.BioMed research international · 2025Article
- Article
- Inhibition mechanism of naphthylphenylamine derivatives acting on the CDC25B dual phosphatase and analysis of the molecular processes involved in the high cytotoxicity exerted by one selected derivative in melanoma cells.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Mutant P53 induces MELK expression by release of wild-type P53-dependent suppression of FOXM1.NPJ breast cancer · 2020Article
- An LTR retrotransposon-derived lncRNA interacts with RNF169 to promote homologous recombination.EMBO reports · 2019Article
- Inhibition of CDC25B With WG-391D Impedes the Tumorigenesis of Ovarian Cancer.Frontiers in oncology · 2019Article
- Identification of CDC25 as a Common Therapeutic Target for Triple-Negative Breast Cancer.Cell reports · 2018Article
- Paeoniflorin induces G2/M cell cycle arrest and caspase-dependent apoptosis through the upregulation of Bcl-2 X-associated protein and downregulation of B-cell lymphoma 2 in human osteosarcoma cells.Molecular medicine reports · 2018Article
- Census and evaluation of p53 target genes.Oncogene · 2017Review
- The PRR11-SKA2 Bidirectional Transcription Unit Is Negatively Regulated by p53 through NF-Y in Lung Cancer Cells.International journal of molecular sciences · 2017Article
- Identification of hub genes and regulatory factors of glioblastoma multiforme subgroups by RNA-seq data analysis.International journal of molecular medicine · 2016Article
- Ovarian tumour growth is characterized by mevalonate pathway gene signature in an orthotopic, syngeneic model of epithelial ovarian cancer.Oncotarget · 2016Article
- NF-Y loss triggers p53 stabilization and apoptosis in HPV18-positive cells by affecting E6 transcription.Oncotarget · 2016Article
- The p53-p21-DREAM-CDE/CHR pathway regulates G2/M cell cycle genes.Nucleic acids research · 2016Article
- Article
- Arabidopsis DPB3-1, a DREB2A interactor, specifically enhances heat stress-induced gene expression by forming a heat stress-specific transcriptional complex with NF-Y subunits.The Plant cell · 2014Article
- p53-dependent gene repression through p21 is mediated by recruitment of E2F4 repression complexes.Oncogene · 2014Article
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Cdc25B phosphatases function as key players in G2/M cell cycle progression by activating the CDK1-cyclinB1 complexes. They also have an essential role in recovery from the G2/M checkpoint activated in response to DNA damage. Overexpression of Cdc25B results in bypass of the G2/M checkpoint and illegitimate entry into mitosis, and also causes replicative stress, leading to genomic instability. Thus, fine-tuning of Cdc25B expression level is critical for correct cell cycle progression and G2 checkpoint recovery. However, the transcriptional regulation of Cdc25B remains largely unknown. Earlier studies have shown that the tumor suppressor p53 overexpression transcriptionally represses Cdc25B; however, the molecular mechanism of this repression has not yet been elucidated, although it was suggested to occur through the induction of p21. Here we show that Cdc25B is downregulated by the basal level of p53 in multiple cell types. This downregulation also occurs in p21-/- cell lines, indicating that p21 is not required for p53-mediated regulation of Cdc25B. Deletion and mutation analyses of the Cdc25B promoter revealed that downregulation by p53 is dependent on the presence of functional Sp1/Sp3 and NF-Y binding sites. Furthermore, chromatin immunoprecipitation analyses show that p53 binds to the Cdc25B promoter and mediates transcriptional attenuation through the Sp1 and NF-Y transcription factors. Our results suggest that the inability to downregulate Cdc25B after loss of p53 might contribute to tumorigenesis.
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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.