Insulin-like growth factor I stimulates transcription of the c-jun proto-oncogene in Balbc 3T3 cells

Chiou, Shean Tai; Chang, Wen Chang

doi:10.1016/0006-291x(92)90513-k

Cited by 13 publications

(4 citation statements)

References 27 publications

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“…It should be noted that the IGF-I-responsive gene portfolio may be cell type-specific or context-dependent. Previous studies demonstrated that IGF-I could up-regulate the expression of some oncogenes, including c-jun, twist, and TEL (40,41). Microarray analysis of IGF-I signaling in 3T3-L1 cells also revealed that IGF-I up-regulated the mitogen heparin-binding epidermal growth factor (42).…”

Section: Discussionmentioning

confidence: 80%

The Reciprocal Regulation of γ-Synuclein and IGF-I Receptor Expression Creates a Circuit That Modulates IGF-I Signaling

Li¹,

Yin²,

Hua³

et al. 2010

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 80%

The Reciprocal Regulation of γ-Synuclein and IGF-I Receptor Expression Creates a Circuit That Modulates IGF-I Signaling

Li¹,

Yin²,

Hua³

et al. 2010

Journal of Biological Chemistry

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“…Inclusion of cycloheximide did not prevent the induction of ␦EF1 and, in fact, resulted in superinduction of the gene. Superinduction in the presence of cycloheximide has been seen for other transcription factors and is most likely due to the loss of a labile repressor of the gene (4,21). ␦EF1 induction is not dependent on concomitant protein synthesis, suggesting that the induction of this gene may well be a direct effect of the estrogen receptor complex.…”

Section: Resultsmentioning

confidence: 85%

Identification of the Novel Player δEF1 in Estrogen Transcriptional Cascades

Chamberlain

Sanders

1999

Molecular and Cellular Biology

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Although many genes are regulated by estrogen, very few have been shown to directly bind the estrogen receptor complex. Therefore, transcriptional cascades probably occur in which the estrogen receptor directly binds to a target gene that encodes another transcription factor that subsequently regulates additional genes. Through the use of a differential display assay, a transcription factor has been identified that may be involved in estrogen transcriptional cascades. This report demonstrates that transcription factor ␦EF1 is induced eightfold by estrogen in the chick oviduct. Furthermore, the regulation by estrogen occurs at the transcriptional level and is likely to be a direct effect of the estrogen receptor complex, as it does not require concomitant protein synthesis. A putative binding site was identified in the 5-flanking region of the chick ovalbumin gene identifying it as a possible target gene for regulation by ␦EF1. Characterization of this binding site revealed that ␦EF1 binds to and regulates the chick ovalbumin gene. Thus, a novel regulatory cascade that is triggered by estrogen has been defined.

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“…Despite the known metabolic functions of these growth factors, insulin and IGF-1 significantly regulated only two genes that are associated with cellular metabolism. Only three of these genes, the Jun oncogene (39,40), ␣-5 integrin (41), and early growth response-1 (42) have been previously reported to be responsive to IGF-1. Fibroblasts are proliferative cells that may not have a well established cellular machinery to mediate metabolic functions, at least compared with other insulin-responsive cell types, such as adipocytes, myocytes, or hepatocytes.…”

Section: Resultsmentioning

confidence: 99%

Insulin and IGF-1 Induce Different Patterns of Gene Expression in Mouse Fibroblast NIH-3T3 Cells: Identification by cDNA Microarray Analysis

Dupont

Khan

et al. 2001

Endocrinology

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The IGF-1 receptor and the related insulin receptor are similar in structure and activate many of the same postreceptor signaling pathways, yet they mediate distinct biological functions. It is still not understood how the specificity of insulin vs. IGF-1 signaling is controlled. In this study, we have used cDNA microarrays to monitor the gene expression patterns that are regulated by insulin and IGF-1. Mouse fibroblast NIH-3T3 cells expressing either the wild-type human IGF receptor or the insulin receptor were stimulated with either IGF-1 or insulin, respectively. Thirty genes, 27 of which were not previously known to be IGF-1 responsive, were up-regulated by IGF-1 but not by insulin. Nine genes, none of which was previously known to be insulin responsive, were up-regulated by insulin but not by IGF-1. The IGF- and insulin-induced regulation of 10 of these genes was confirmed by Northern blot analysis. Interestingly, more than half of the genes up-regulated by IGF-1 are associated with mitogenesis and differentiation, whereas none of the genes specifically up-regulated by insulin are associated with these processes. Our results indicate that under the conditions used in this study, IGF-1 is a more potent activator of the mitogenic pathway than insulin in mouse fibroblast NIH-3T3 cells.

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Insulin-like growth factor I stimulates transcription of the c-jun proto-oncogene in Balbc 3T3 cells

Cited by 13 publications

References 27 publications

The Reciprocal Regulation of γ-Synuclein and IGF-I Receptor Expression Creates a Circuit That Modulates IGF-I Signaling

The Reciprocal Regulation of γ-Synuclein and IGF-I Receptor Expression Creates a Circuit That Modulates IGF-I Signaling

Identification of the Novel Player δEF1 in Estrogen Transcriptional Cascades

Insulin and IGF-1 Induce Different Patterns of Gene Expression in Mouse Fibroblast NIH-3T3 Cells: Identification by cDNA Microarray Analysis

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