ArticleOncogene2009
Pro-proliferative FoxM1 is a target of p53-mediated repression.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 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
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
102 citing papers in PubMed, 161 citations in OpenAlex.
- Trial
- A microprotein encoded by FERMT3 modulates endothelial cell protein catabolism and induces cell cycle arrest and senescence.Cell communication and signaling : CCS · 2026Article
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- HMMR in human cancers: regulatory mechanism and biological function.Journal of translational medicine · 2025Review
- Article
- Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.Cell proliferation · 2025Article
- NOSH-aspirin (NBS-1120) inhibits estrogen receptor-negative breast cancer in vitro and in vivo by modulating redox-sensitive signaling pathways.The Journal of pharmacology and experimental therapeutics · 2025Article
- Baicalein Inhibits Proliferation, Migration, and Invasion of Mesothelioma Cells Through the p53-FOXM1 Signaling Axis.Cancer management and research · 2025Article
- Therapeutic Landscape of FOXM1 in Triple-Negative Breast Cancer and Aggressive Solid Cancers.Cancers · 2024Review
- ESR1 and p53 interactome alteration defines mechanisms of tamoxifen response in luminal breast cancer.iScience · 2024Article
- Oncogenic Pathways and Targeted Therapies in Ovarian Cancer.Biomolecules · 2024Review
- Mechanistic Insights about Sorafenib-, Valproic Acid- and Metformin-Induced Cell Death in Hepatocellular Carcinoma.International journal of molecular sciences · 2024Review
- FOXM1, MEK, and CDK4/6: New Targets for Malignant Peripheral Nerve Sheath Tumor Therapy.International journal of molecular sciences · 2023Review
- Inhibition of USP7 induces p53-independent tumor growth suppression in triple-negative breast cancers by destabilizing FOXM1.Cell death and differentiation · 2023Article
- FOXM1: A small fox that makes more tracks for cancer progression and metastasis.Seminars in cancer biology · 2023Review
- The Role of Polo-Like Kinase 1 in Regulating the Forkhead Box Family Transcription Factors.Cells · 2023Review
- Heat shock proteins and cancer: The FoxM1 connection.Biochemical pharmacology · 2023Review
- Targeting TACC3 represents a novel vulnerability in highly aggressive breast cancers with centrosome amplification.Cell death and differentiation · 2023Article
- MicroRNA-1 attenuates the growth and metastasis of small cell lung cancer through CXCR4/FOXM1/RRM2 axis.Molecular cancer · 2023Article
42 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor protein acts as a transcription factor to modulate cellular responses to a wide variety of stresses. In this study we show that p53 is required for the downregulation of FoxM1, an essential transcription factor that regulates many G2/M-specific genes and is overexpressed in a multitude of solid tumors. After DNA damage, p53 facilitates the repression of FoxM1 mRNA, which is accompanied by a decrease in FoxM1 protein levels. In cells with reduced p53 expression, FoxM1 is upregulated after DNA damage. Nutlin, a small-molecule activator of p53, suppresses FoxM1 levels in two cell lines in which DNA damage facilitates only mild repression. Mechanistically, p53-mediated inhibition of FoxM1 is partially p21 and retinoblastoma (Rb) family dependent, although in some cases p21-independent repression of FoxM1 was also observed. The importance of FoxM1 to cell fate was indicated by the observation that G2/M arrest follows FoxM1 ablation. Finally, our results indicate a potential contribution of p53-mediated repression of FoxM1 for maintenance of a stable G2 arrest.
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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.