ArticleMolecular and cellular biology1999
Insulin-like growth factor I synergizes with interleukin 4 for hematopoietic cell proliferation independent of insulin receptor substrate expression.
Article in Molecular and cellular biology, 1999. 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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Who cites it
19 citing papers in PubMed, 55 citations in OpenAlex.
- Pleiotropic Effect of Hormone Insulin-Like Growth Factor-I in Immune Response and Pathogenesis in Leishmaniases.Journal of immunology research · 2021Review
- Insulin-like Growth Factor 1 Supports a Pulmonary Niche that Promotes Type 3 Innate Lymphoid Cell Development in Newborn Lungs.Immunity · 2020Article
- Insulin Substrate Receptor (IRS) proteins in normal and malignant hematopoiesis.Clinics (Sao Paulo, Brazil) · 2018Review
- Insulin-Like Growth Factor-I as an Effector Element of the Cytokine IL-4 in the Development of aMediators of inflammation · 2018Article
- The insulin-like growth factor-I receptor (IGF-IR) in breast cancer: biology and treatment strategies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Interactions between Myc and Mediators of Inflammation in Chronic Liver Diseases.Mediators of inflammation · 2015Review
- Upregulation of IGF1R by mutant RAS in leukemia and potentiation of RAS signaling inhibitors by small-molecule inhibition of IGF1R.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Insulin-like growth factor 1 mitigates hematopoietic toxicity after lethal total body irradiation.International journal of radiation oncology, biology, physics · 2013Article
- STAT6 expression in glioblastoma promotes invasive growth.BMC cancer · 2011Article
- IL-6 promotes prostate tumorigenesis and progression through autocrine cross-activation of IGF-IR.Oncogene · 2011Article
- IL-4R drives dedifferentiation, mitogenesis, and metastasis in rhabdomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Gab1 mediates hepatocyte growth factor-stimulated mitogenicity and morphogenesis in multipotent myeloid cells.Journal of cellular biochemistry · 2010Article
- Insulin-like growth factor-I regulation of immune function: a potential therapeutic target in autoimmune diseases?Pharmacological reviews · 2010Review
- Detection of a functional hybrid receptor gammac/GM-CSFRbeta in human hematopoietic CD34+ cells.The Journal of experimental medicine · 2003Article
- Mitogenic synergy through multilevel convergence of hepatocyte growth factor and interleukin-4 signaling pathways.Oncogene · 2002Article
- Regulation of Id gene expression by type I insulin-like growth factor: roles of Stat3 and the tyrosine 950 residue of the receptor.Molecular and cellular biology · 2001Article
- IGF-I receptor signalling in transformation and differentiation.Molecular pathology : MP · 2001Review
- Review
- Cooperative transformation of 32D cells by the combined expression of IRS-1 and V-Ha-Ras.Oncogene · 2000Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we investigated the potential role of insulin-like growth factor I (IGF-I) receptor (IGF-IR) in cell proliferation by overexpressing it in 32D myeloid progenitor cells. The overexpression of IGF-IR caused the transfectants to proliferate in response to IGF-I in the absence of insulin receptor substrate (IRS) expression. The activation of overexpressed wild-type IGF-IR, but not that of an ATP-binding mutant of IGF-IR, resulted in the increased tyrosine phosphorylation of several intracellular proteins, including SHC, Src homology 2-containing inositol-5-phosphatase, protein kinase C-delta, and Erk2. Grb2 association with SHC and mitogen-activated protein kinase (MAPK) activity was also enhanced in response to IGF-I stimulation. Interestingly, the stimulation of the IGF-IR transfectants with interleukin 4 (IL-4) also resulted in strong mitogenesis independent of IRS expression. Moreover, IGF-I and/or IL-4 induced long-term cell growth of the IGF-IR transfectants. IL-4 was able to synergize with IGF-I for DNA synthesis, even in the parental 32D cells and a pro-B-cell line, Baf3, indicating the physiological importance of the two growth factors in hematopoietic cell proliferation. IL-4 stimulation of the IGF-IR transfectants resulted in enhanced tyrosine phosphorylation of SHC, Erk2, and signal transducer and activator of transcription 6 (STAT6) proteins. Both IL-4 and IGF-I were able to induce c-myc early response gene expression, and this expression was maximal in the presence of both factors. Finally, we demonstrated that a MAPK kinase inhibitor was able to suppress mitogenesis of the IGF-IR transfectants in response to IGF-I and/or IL-4. Together, our results suggest that IL-4 synergizes with IGF-I for hematopoietic cell proliferation, likely through cross talk between SHC/Grb2/MAPK and STAT6 pathways and through c-myc gene up-regulation.
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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.