ArticleOncogene2003
Inhibition of Egr-1 expression reverses transformation of prostate cancer cells in vitro and in vivo.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
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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
50 citing papers in PubMed, 103 citations in OpenAlex.
- Uncovering genes driving developmental stage progression in prostate cancer through spatial transcriptomics.Genes & diseases · 2026Article
- Melatonin Alleviates Oxidative Stress Induced by HAntioxidants (Basel, Switzerland) · 2022Article
- Cytoskeletal dysregulation and neurodegenerative disease: Formation, monitoring, and inhibition of cofilin-actin rods.Frontiers in cellular neuroscience · 2022Review
- miR-377-3p-Mediated EGR1 Downregulation Promotes B[a]P-Induced Lung Tumorigenesis by Wnt/Beta-Catenin Transduction.Frontiers in oncology · 2021Article
- Expression and prognostic value of the transcription factors EGR1 and EGR3 in gliomas.Scientific reports · 2020Article
- Differential functions of ERK1 and ERK2 in lung metastasis processes in triple-negative breast cancer.Scientific reports · 2020Article
- The role of HOPX in normal tissues and tumor progression.Bioscience reports · 2020Review
- Network-Based Approach to Identify the Antiproliferative Mechanisms of Bruceine D in Breast Cancer From the Cancer Genome Atlas.Frontiers in oncology · 2020Article
- Article
- Identification, Characterization, and Regulatory Mechanisms of a Novel EGR1 Splicing Isoform.International journal of molecular sciences · 2019Article
- GCN5 inhibition prevents IL-6-induced prostate cancer metastases through PI3K/PTEN/Akt signaling by inactivating Egr-1.Bioscience reports · 2018Article
- ISG15 Promotes ERK1 ISGylation, CD8+ T Cell Activation and Suppresses Ovarian Cancer Progression.Cancers · 2018Article
- Transcriptional Landscape of PARs in Epithelial Malignancies.International journal of molecular sciences · 2018Review
- Spatial maps of prostate cancer transcriptomes reveal an unexplored landscape of heterogeneity.Nature communications · 2018Article
- Article
- Egr-1 regulates RTA transcription through a cooperative involvement of transcriptional regulators.Oncotarget · 2017Article
- Impairment of the activin A autocrine loop by lopinavir reduces self-renewal of distinct human adipose progenitors.Scientific reports · 2017Article
- Radiation Induced Apoptosis of Murine Bone Marrow Cells Is Independent of Early Growth Response 1 (EGR1).PloS one · 2017Article
- A Positive Feed-forward Loop Associating EGR1 and PDGFA Promotes Proliferation and Self-renewal in Glioblastoma Stem Cells.The Journal of biological chemistry · 2016Article
- Epigenetics Reactivation of Nrf2 in Prostate TRAMP C1 Cells by Curcumin Analogue FN1.Chemical research in toxicology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Transcription factor early growth response-1 (Egr-1) is a crucial regulator of cell growth, differentiation and survival. Several observations suggest that Egr-1 is growth promoting in prostate cancer cells and that blocking its function may impede cancer progression. To test this hypothesis, we developed phosphorothioate antisense oligonucleotides that efficiently inhibit Egr-1 expression without altering the expression of other family members Egr-2, Egr-3 and Egr-4. In TRAMP mouse-derived prostate cancer cell lines, our optimal antisense oligonucleotide decreased the expression of the Egr-1 target gene transforming growth factor-beta1 whereas a control oligonucleotide had no effect, indicating that the antisense blocked Egr-1 function as a transcription factor. The antisense oligonucleotide deregulated cell cycle progression and decreased proliferation of the three TRAMP cell lines by an average of 54+/-3%. Both colony formation and growth in soft agar were inhibited by the antisense oligonucleotide. When TRAMP mice were treated systemically for 10 weeks, the incidence of palpable tumors at 32 weeks of age in untreated mice or mice injected with the control scramble oligonucleotide was 87%, whereas incidence of tumors in antisense-Egr-1-treated mice was significantly reduced to 37% (P=0.026). Thus, Egr-1 plays a functional role in the transformed phenotype and may represent a valid target for prostate cancer therapy.
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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.