ArticleOncogene2000
Cooperative transformation of 32D cells by the combined expression of IRS-1 and V-Ha-Ras.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Epigenetic regulation of insulin-like growth factor axis in hepatocellular carcinoma.World journal of gastroenterology · 2016Review
- Type 1 Insulin-Like Growth Factor Receptor/Insulin Receptor Substrate 1 Signaling Confers Pathogenic Activity on Breast Tumor Cells Lacking REST.Molecular and cellular biology · 2015Article
- IRS1 regulation by Wnt/beta-catenin signaling and varied contribution of IRS1 to the neoplastic phenotype.The Journal of biological chemistry · 2010Article
- Expression and function of the insulin receptor substrate proteins in cancer.Cell communication and signaling : CCS · 2009Article
- Igf1r as a therapeutic target in a mouse model of basal-like breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Insulin receptor substrates (IRSs) and breast tumorigenesis.Journal of mammary gland biology and neoplasia · 2008Review
- Transgenic overexpression of insulin receptor substrate 1 in hepatocytes enhances hepatocellular proliferation in young mice only.Hepatology research : the official journal of the Japan Society of Hepatology · 2008Article
- Nuclear insulin receptor substrate-1 activates promoters of cell cycle progression genes.Oncogene · 2008Article
- The phosphoinositide 3-kinase pathway in human cancer: genetic alterations and therapeutic implications.Current genomics · 2007Article
- Article
- Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors.Leukemia · 2006Article
- An unusual H-Ras mutant isolated from a human multiple myeloma line leads to transformation and factor-independent cell growth.Oncogene · 2003Article
- 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
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
32D cells expressing v-Ha-Ras fail to show a transformed phenotype. Since Ras requires an active IGF-1R for transformation of fibroblasts, we asked whether expression of IRS-1 or Shc (two of the major substrates of the IGF-1R) could co-operate with oncogenic Ras in transforming 32D cells. We find that IRS-1, but not Shc, in combination with v-Ha-Ras generates a fully transformed phenotype in 32D cells. 32D cells expressing both IRS-1 and v-Ha-Ras (32D/IRS1/Ras) survive and proliferate in the absence of IL-3, do not undergo granulocytic differentiation in the presence of G-CSF and form tumors in nu/nu and syngeneic mice. In contrast, 32D cells expressing singly IRS-1 or v-Ha-Ras exhibit only a block in differentiation capacity. Over-expression of Shc proteins, by itself, promotes differentiation of 32D cells. Concomitant expression of IRS-1 and v-Ha-Ras synergistically phosphorylates ERK-1 and ERK-2 whereas a MEK inhibitor rapidly induces death of 32D/IRS1/Ras transformed cells. Furthermore, transformed 32D/IRS1/Ras cells display high levels of PI3-K activation and undergo rapid apoptosis when exposed to PI3-K inhibitors. The data indicate that: (1) a fully transformed phenotype in 32D cells is generated when a block in differentiation (v-Ha-Ras) is coupled with another differentiation block (IRS-1); (2) PI3-K and MAPK activity are required for the survival of transformed cells; (3) the signals generated by IRS-1 and oncogenic Ras converge on ERK and PI3-K resulting in high levels of activation.
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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.