ArticleNucleic acids research2001
PEA3 sites within the progression elevated gene-3 (PEG-3) promoter and mitogen-activated protein kinase contribute to differential PEG-3 expression in Ha-ras and v-raf oncogene transformed rat embryo cells.
Article in Nucleic acids research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 33 citations in OpenAlex.
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- Selected approaches for rational drug design and high throughput screening to identify anti-cancer molecules.Anti-cancer agents in medicinal chemistry · 2012Review
- Chapter One---Cancer terminator viruses and approaches for enhancing therapeutic outcomes.Advances in cancer research · 2012Review
- The role of Pea3 group transcription factors in esophageal squamous cell carcinoma.The American journal of pathology · 2011Article
- IL-6 promotes prostate tumorigenesis and progression through autocrine cross-activation of IGF-IR.Oncogene · 2011Article
- Developing an effective gene therapy for prostate cancer: New technologies with potential to translate from the laboratory into the clinic.Discovery medicine · 2011Review
- Inhibition of AP-1 by SARI negatively regulates transformation progression mediated by CCN1.Oncogene · 2010Article
- Cloning and characterization of SARI (suppressor of AP-1, regulated by IFN).Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- A cancer terminator virus eradicates both primary and distant human melanomas.Cancer gene therapy · 2008Article
- Astrocyte elevated gene-1 (AEG-1) is a target gene of oncogenic Ha-ras requiring phosphatidylinositol 3-kinase and c-Myc.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Ionizing radiation enhances adenoviral vector expressing mda-7/IL-24-mediated apoptosis in human ovarian cancer.Journal of cellular physiology · 2006Article
- Dual cancer-specific targeting strategy cures primary and distant breast carcinomas in nude mice.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- The antagonistic regulation of human MUC4 and ErbB-2 genes by the Ets protein PEA3 in pancreatic cancer cells: implications for the proliferation/differentiation balance in the cells.The Biochemical journal · 2005Article
- Targeting gene expression selectively in cancer cells by using the progression-elevated gene-3 promoter.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Insights into glutamate transport regulation in human astrocytes: cloning of the promoter for excitatory amino acid transporter 2 (EAAT2).Proceedings of the National Academy of Sciences of the United States of America · 2003Article
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8 authors at 1 institution in 1 country.
Funding
Abstract
Transformation of normal cloned rat embryo fibroblast (CREF) cells with cellular oncogenes results in acquisition of anchorage-independent growth and oncogenic potential in nude mice. These cellular changes correlate with an induction in the expression of a cancer progression-promoting gene, progression elevated gene-3 (PEG-3). To define the mechanism of activation of PEG-3 as a function of transformation by the Ha-ras and v-raf oncogenes, evaluations of the signaling and transcriptional regulation of the approximately 2.0 kb promoter region of the PEG-3 gene, PEG-Prom, was undertaken. The full-length and various mutated regions of the PEG-Prom were linked to a luciferase reporter construct and tested for promoter activity in CREF and oncogene-transformed CREF cells. An analysis was also performed using CREF cells doubly transformed with Ha-ras and the Ha-ras specific suppressor gene Krev-1, which inhibits the transformed phenotype in vitro. These assays document an association between expression of the transcription regulator PEA3 and PEG-3. The levels of PEA3 and PEG-3 RNA and proteins are elevated in the oncogenically transformed CREF cells, and reduced in transformation and tumorigenic suppressed Ha-ras/Krev-1 doubly transformed CREF cells. Enhanced tumorigenic behavior, PEG-3 promoter function and PEG-3 expression in Ha-ras transformed cells were all dependent upon increased activity within the mitogen-activated protein kinase (MAPK) pathway. Electrophoretic mobility shift assays and DNase I footprinting experiments indicate that PEA3 binds to sites within the PEG-Prom in transformed rodent cells in an area adjacent to the TATA box in a MAPK-dependent fashion. These findings demonstrate an association between Ha-ras and v-raf transformation of CREF cells with elevated PEA3 and PEG-3 expression, and they implicate MAPK signaling via PEA3 as a signaling cascade involved in activation of the PEG-Prom.
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