ArticleOncogene2010
Mutant p53 initiates a feedback loop that involves Egr-1/EGF receptor/ERK in prostate cancer cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 81 citations in OpenAlex.
- Mutant p53 Regulates Pyruvate Dehydrogenase Kinase 1 (PDK1) to Promote Proliferation and Migration in Breast Cancer.Cancer science · 2026Article
- Sensitizing Immune-Refractory Ovarian Tumors via p53 Mutation-Tailored Immunotherapy.bioRxiv : the preprint server for biology · 2025Article
- Review
- Dysregulated Signalling Pathways Driving Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
- Article
- Effect of KRAS mutations and p53 expression on the postoperative prognosis of patients with colorectal cancer.Molecular genetics & genomic medicine · 2022Article
- Characterization of EGR-1 Expression in the Auditory Cortex Following Kanamycin-Induced Hearing Loss in Mice.Journal of molecular neuroscience : MN · 2021Article
- Article
- Disrupting biological sensors of force promotes tissue regeneration in large organisms.Nature communications · 2021Article
- Gain-of-Function Mutant TP53 R248Q Overexpressed in Epithelial Ovarian Carcinoma Alters AKT-Dependent Regulation of Intercellular Trafficking in Responses to EGFR/MDM2 Inhibitor.International journal of molecular sciences · 2021Article
- Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21.IUBMB life · 2021Article
- Expression of UDP GlucuronosyltransferasesEpigenetics · 2021Article
- TP53, SPOP and PIK3CA Genes Status in Prostate Cancer.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Review
- Dysregulation of Signaling Pathways Due to Differentially Expressed Genes From the B-Cell Transcriptomes of Systemic Lupus Erythematosus Patients - A Bioinformatics Approach.Frontiers in bioengineering and biotechnology · 2020Article
- Friend or foe, the role of EGR-1 in cancer.Medical oncology (Northwood, London, England) · 2019Review
- Article
- Repurposing EGFR Inhibitor Utility in Colorectal Cancer in MutantCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019Article
- Beyond EGFR inhibition: multilateral combat strategies to stop the progression of head and neck cancer.Experimental & molecular medicine · 2019Review
- On the influence of cannabinoids on cell morphology and motility of glioblastoma cells.PloS one · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Early growth response-1 (Egr-1) is overexpressed in human prostate tumors and contributes to cancer progression. On the other hand, mutation of p53 is associated with advanced prostate cancer, as well as with metastasis and hormone independence. This study shows that in prostate cell lines in culture, Egr-1 overexpression correlated with an alteration of p53 activity because of the expression of SV40 large T-antigen or because of a mutation in the TP53 gene. In cells containing altered p53 activity, Egr-1 expression was abolished by pharmacological inhibition or RNAi silencing of p53. Although forced expression of wild-type p53 was not sufficient to trigger Egr-1 transcription, four different mutants of p53 were shown to induce Egr-1. Direct binding of p53 to the EGR1 promoter could not be detected. Instead, Egr-1 transcription was driven by the ERK1/2 pathway, as it was abrogated by specific inhibitors of MEK. Egr-1 increased the transcription of HB-EGF (epidermal growth factor), amphiregulin and epiregulin, resulting in autocrine activation of the EGF receptor (EGFR) and downstream MEK/ERK cascade. Thus, mutant p53 initiates a feedback loop that involves ERK1/2-mediated transactivation of Egr-1, which in turn increases the secretion of EGFR ligands and stimulates the EGFR signaling pathway. Finally, p53 may further regulate this feedback loop by altering the level of EGFR expression.
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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.