ArticlePLoS genetics2014
p53 requires the stress sensor USF1 to direct appropriate cell fate decision.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- The dark side of the light (UVA): melanoma microenvironment and cell survival strategies.Cell death discovery · 2025Article
- Upstream stimulating factor 1 (USF1) -202 G/A polymorphism and serum levels of USF1 and USF2 are associated with gastric cancer risk: a case control study.Journal of cancer research and clinical oncology · 2025Article
- Knockdown of USF1 and USF2 drives prolonged changes in the gene expression response of M12-5B3 cells to DNA damage.PloS one · 2025Article
- A natural variation-based screen in mouse cells reveals USF2 as a regulator of the DNA damage response and cellular senescence.G3 (Bethesda, Md.) · 2023Article
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- E-box binding transcription factors in cancer.Frontiers in oncology · 2023Review
- Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022Review
- Targeting Post-Translational Regulation of p53 in Colorectal Cancer by Exploiting Vulnerabilities in the p53-MDM2 Axis.Cancers · 2022Review
- ADAM9 functions as a transcriptional regulator to drive angiogenesis in esophageal squamous cell carcinoma.International journal of biological sciences · 2021Article
- Article
- Role of Flavonoids in the Prevention of AhR-Dependent Resistance During Treatment with BRAF Inhibitors.International journal of molecular sciences · 2020Article
- Article
- A comprehensive analysis of coding and non-coding transcriptomic changes in cutaneous squamous cell carcinoma.Scientific reports · 2020Article
- TopControl: A Tool to Prioritize Candidate Disease-associated Genes based on Topological Network Features.Scientific reports · 2019Article
- TGF-β1-p53 cooperativity regulates a profibrotic genomic program in the kidney: molecular mechanisms and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Review
- Article
- Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis.Molecular therapy. Nucleic acids · 2019Article
- UV-B-activated B16 melanoma cells or HaCaT keratinocytes accelerate signaling pathways associated with melanogenesis via ANGPTL 2 induction, an activity antagonized by Chrysanthemum extract.Experimental dermatology · 2019Article
- Sustained activation of the Aryl hydrocarbon Receptor transcription factor promotes resistance to BRAF-inhibitors in melanoma.Nature communications · 2018Article
- Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genomic instability is a major hallmark of cancer. To maintain genomic integrity, cells are equipped with dedicated sensors to monitor DNA repair or to force damaged cells into death programs. The tumor suppressor p53 is central in this process. Here, we report that the ubiquitous transcription factor Upstream Stimulatory factor 1 (USF1) coordinates p53 function in making proper cell fate decisions. USF1 stabilizes the p53 protein and promotes a transient cell cycle arrest, in the presence of DNA damage. Thus, cell proliferation is maintained inappropriately in Usf1 KO mice and in USF1-deficient melanoma cells challenged by genotoxic stress. We further demonstrate that the loss of USF1 compromises p53 stability by enhancing p53-MDM2 complex formation and MDM2-mediated degradation of p53. In USF1-deficient cells, the level of p53 can be restored by the re-expression of full-length USF1 protein similarly to what is observed using Nutlin-3, a specific inhibitor that prevents p53-MDM2 interaction. Consistent with a new function for USF1, a USF1 truncated protein lacking its DNA-binding and transactivation domains can also restore the induction and activity of p53. These findings establish that p53 function requires the ubiquitous stress sensor USF1 for appropriate cell fate decisions in response to DNA-damage. They underscore the new role of USF1 and give new clues of how p53 loss of function can occur in any cell type. Finally, these findings are of clinical relevance because they provide new therapeutic prospects in stabilizing and reactivating the p53 pathway.
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