ArticleMolecular and cellular biology1995
Inhibition of cellular proliferation by the Wilms' tumor suppressor WT1 is associated with suppression of insulin-like growth factor I receptor gene expression.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 112 citations in OpenAlex.
- Article
- Insulin-like Growth Factor 1 Signaling Axis Meets p53 Genome Protection Pathways.Frontiers in oncology · 2016Review
- Risk of Neoplasia in Pediatric Patients Receiving Growth Hormone Therapy--A Report From the Pediatric Endocrine Society Drug and Therapeutics Committee.The Journal of clinical endocrinology and metabolism · 2015Review
- Mechanisms of transcriptional regulation by WT1 (Wilms' tumour 1).The Biochemical journal · 2014Review
- Targeting the insulin growth factor receptor 1.Hematology/oncology clinics of North America · 2012Review
- Tumor suppressors govern insulin-like growth factor signaling pathways: implications in metabolism and cancer.Oncogene · 2012Review
- The role of IGF-1R in pediatric malignancies.The oncologist · 2009Review
- Pediatric developmental therapies: interesting new drugs now in early-stage clinical trials.Current oncology reports · 2008Review
- In silico regulatory analysis for exploring human disease progression.Biology direct · 2008Article
- Role of insulin-like growth factor 1 receptor signalling in cancer.British journal of cancer · 2005Review
- The ELAV RNA-stability factor HuR binds the 5'-untranslated region of the human IGF-IR transcript and differentially represses cap-dependent and IRES-mediated translation.Nucleic acids research · 2005Article
- Cancer.Advances in experimental medicine and biology · 2005Review
- WT1 is a modifier of the Pax2 mutant phenotype: cooperation and interaction between WT1 and Pax2.Oncogene · 2003Article
- Transcriptional regulation of IGF-I receptor gene expression by novel isoforms of the EWS-WT1 fusion protein.Oncogene · 2002Article
- Forced expression of the Wilms tumor 1 (WT1) gene inhibits proliferation of human hematopoietic CD34(+) progenitor cells.Leukemia · 2001Article
- Review
- WT1 expression induces features of renal epithelial differentiation in mesenchymal fibroblasts.Oncogene · 1999Article
- Tumor suppressor p53 can participate in transcriptional induction of the GADD45 promoter in the absence of direct DNA binding.Molecular and cellular biology · 1998Article
- Wilms' tumour-suppressor protein isoforms have opposite effects on Igf2 expression in primary embryonic cells, independently of p53 genotype.British journal of cancer · 1998Article
- Insulin-like growth factor I receptor signaling in transformation by src oncogenes.Molecular and cellular biology · 1997Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We have investigated the regulation of the insulin-like growth factor I receptor (IGF-I-R) gene promoter by the Wilms' tumor suppressor WT1 in intact cells. The levels of endogenous IGF-I-R mRNA and the activity of IGF-I-R gene promoter fragments in luciferase reporter constructs were found to be significantly higher in G401 cells (a Wilms' tumor-derived cell line lacking detectable WT1 mRNA) than in 293 cells (a human embryonic kidney cell line which expresses significant levels of WT1 mRNA). To study whether WT1 could suppress the expression of the endogenous IGF-I-R gene, WT1-negative G401 cells were stably transfected with a WT1 expression vector. Expression of WT1 mRNA in G401 cells resulted in a significant decrease in the rate of cellular proliferation, which was associated with a reduction in the levels of IGF-I-R mRNA, promoter activity, and ligand binding and with a reduction in IGF-I-stimulated cellular proliferation, thymidine incorporation, and anchorage-independent growth. These data suggest that a major aspect of the action of the WT1 tumor suppressor is the repression of IGF-I-R gene expression.
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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.