ArticleThe EMBO journal2006
Suppression of Egr-1 transcription through targeting of the serum response factor by oncogenic H-Ras.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 49 citations in OpenAlex.
- CCT3-Gut · 2022Article
- Nuclear-capture of endosomes depletes nuclear G-actin to promote SRF/MRTF activation and cancer cell invasion.Nature communications · 2021Article
- Soluble Epoxide Hydrolase Inhibitors Regulate Ischemic Arrhythmia by Targeting MicroRNA-1.Frontiers in physiology · 2021Article
- Mechanistic Analysis of an Extracellular Signal-Regulated Kinase 2-Interacting Compound that Inhibits Mutant BRAF-Expressing Melanoma Cells by Inducing Oxidative Stress.The Journal of pharmacology and experimental therapeutics · 2021Article
- MiR-125b-2-3p associates with prognosis of ccRCC through promoting tumor metastasis via targeting EGR1.American journal of translational research · 2020Article
- An Arf-Egr-C/EBPβ pathway linked to ras-induced senescence and cancer.Molecular and cellular biology · 2015Article
- Constitutively active Ras negatively regulates Erk MAP kinase through induction of MAP kinase phosphatase 3 (MKP3) in NIH3T3 cells.BMB reports · 2014Article
- Mutant p53 initiates a feedback loop that involves Egr-1/EGF receptor/ERK in prostate cancer cells.Oncogene · 2010Article
- Egr-1 is necessary for fibroblast growth factor-2-induced transcriptional activation of the glial cell line-derived neurotrophic factor in murine astrocytes.The Journal of biological chemistry · 2009Article
- RasV12-mediated down-regulation of CCAAT/enhancer binding protein beta in immortalized fibroblasts requires loss of p19Arf and facilitates bypass of oncogene-induced senescence.Cancer research · 2009Article
- PTEN regulation by Akt-EGR1-ARF-PTEN axis.The EMBO journal · 2009Article
- Efficient serum-free derivation of oligodendrocyte precursors from neural stem cell-enriched cultures.Stem cells (Dayton, Ohio) · 2009Article
- Combined effects of radiotherapy and endostatin gene therapy in melanoma tumor model.Radiation and environmental biophysics · 2008Article
- Promoter-independent regulation of vimentin expression in mammary epithelial cells by val(12)ras and TGFbeta.Experimental cell research · 2007Article
- Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders.Blood · 2007Article
- The cytoskeleton-associated PDZ-LIM protein, ALP, acts on serum response factor activity to regulate muscle differentiation.Molecular biology of the cell · 2007Article
- Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor Egr-1 functions as a key regulator in cellular growth, differentiation, and apoptosis. The loss of Egr-1 expression is closely associated with tumor development, although the molecular mechanism behind the suppression of Egr-1 is largely unknown. In this report, we show that growth factor-induced transcriptional activation of Egr-1 gene is downregulated by chronic expression of oncogenic H-Ras in NIH3T3 fibroblasts. Our results demonstrate that phosphoinositide 3-kinase (PI3K) signaling is necessary for oncogenic H-Ras-mediated reduction of Egr-1 gene expression. Aberrant activation of PI3K signaling by oncogenic Ras decreased the level of serum response factor (SRF) protein through the acceleration of proteolysis, which resulted in decreased SRF binding to the serum response element (SRE) sites within the Egr-1 promoter, leading to the suppression of Egr-1 transcription. Inhibition of PI3K signaling restored the downregulation of SRF and Egr-1 expression caused by oncogenic Ras. Our findings suggest a novel signaling mechanism by which prolonged activation of oncogenic H-Ras can trigger the loss of tumor suppressor Egr-1 through the PI3K pathway in NIH3T3 fibroblast model cell lines.
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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.