Gene interactions and pathways from curated databases and text-mining

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IGF1 — TP53

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: IGF1 → TP53 (decreases, TP53 Activity)
    Evidence: IGFbPs limit IGF access to IGF1R, thereby attenuating the bioactivity of these growth factors33. The tumour suppressor p53 (REF. 34), as well as many growth inhibitors including vitamin d35, anti- oestrogens36, retinoids37, and transforming growth factor-? (TGF?37), reduce IGF bioactivity by increasing the secretion of IGFbPs33.

Text-mined interactions from Literome

Girnita et al., Cancer Res 2000 (Melanoma) : Taken together, our results suggest that up-regulation of IGF-IR as a result of expression of aberrant p53 may be important for the growth and survival of malignant cells
Idelman et al., J Biol Chem 2003 (Bone Neoplasms...) : WT1 splice variants lacking a KTS insert between zinc fingers 3 and 4 suppressed IGF-IR promoter activity in the absence of p53 or in the presence of wild-type p53 ... In the presence of mutant p53 , WT1 can not repress the IGF-IR promoter
Lee et al., Mol Cell Endocrinol 2003 (Carcinoma, Hepatocellular) : p53mt249 increased the number of IGF-II binding sites with no change in the affinity of IGF-IR
Harms et al., Mol Cell Biol 2005 : Through the use of engineered deletion mutants, we found that activation domain 2 is required for induction of the proapoptotic target gene insulin-like growth factor binding protein 3 ( IGFBP3 ) by p53 and that the basic domain inhibits induction of this gene by p53
Clark et al., Int J Cancer 2005 (Breast Neoplasms) : Although IGF-I acutely suppressed the p53 response to both agents, it subsequently enhanced the chronic increase in p53 and p21 ( WAF1/Cip1 ), resulting in cell cycle arrest ; however, no apoptosis was observed
Ma et al., J Exp Clin Cancer Res 2006 (Adenocarcinoma...) : It was also found that the absence of mutant p53 affected the signal transduction of TGFbeta/BMP pathway mainly by up-regulating the expression of BMP superfamily cytokine growth differentiation factor 9 (GDF9), activin superfamily cytokine inhibin beta B (INHBB), smads target genes insulin-like growth factor binding protein 3 ( IGFBP3 ) and involucrin (IVL)
Adamson et al., Altern Lab Anim 2007 : Under these conditions, IGF-1 may increase p53 expression to restrain abnormal cell proliferation
Bocchetta et al., Cancer Res 2008 (Cell Transformation, Neoplastic) : The SV40 large T antigen-p53 complexes bind and activate the insulin-like growth factor-I promoter stimulating cell growth ... We found that in human cells, Tag-p53 complexes regulate transcription of the insulin-like growth factor I (IGF-I) gene by binding to the IGF-I promoter together with pRb and p300
Scrable et al., Exp Gerontol 2009 (Starvation) : Running on empty : how p53 controls INS/IGF signaling and affects life span
Li et al., Rejuvenation Res 2008 (Calcium Signaling...) : Our data suggest that regulation of Akt, p53 , adenosine monophosphate activated protein kinase ( AMPK ) phosphorylation, and Klotho may play a role, at least in part, in IGF-1 deficiency induced `` desensitization '' of cardiac aging
Kuramoto et al., Acta Med Okayama 2008 (Cervical Intraepithelial Neoplasia...) : It is postulated that a decrease of p53 protein levels due to human papillomavirus ( HPV ) infection may contribute to the up-regulation of IGF-IR expression in cervical cancer cells because transcription of IGF-IR is strictly down-regulated by p53
Goetz et al., Oncogene 2011 (Genomic Instability...) : Here, we show that activation of Ataxia telangiectasia mutated kinase ( ATM ) by endogenous or exogenous forms of DNA damage was required to relieve basal repression of IGF-1 transcription by the p53/NF-YA complex, leading to sCLU expression
Attias-Geva et al., Eur J Cancer 2012 (Cystadenocarcinoma, Serous...) : In addition, using USC derived cell lines we provide evidence that p53 regulates IGF-IR gene expression via a mechanism that involves repression of the IGF-IR promoter ... In summary, we provide evidence that p53 regulates IGF-IR gene expression in USC cells via a mechanism that involves repression of the IGF-IR promoter
Chen et al., Endocrinology 1995 : In order to understand the mechanisms through which IGF I regulates cardiac muscle growth, we have studied the effects of IGF I on inhibitory pathways involving p53 and WAF1 in cultured cardiac muscle cell line H9C2
Werner et al., Proc Natl Acad Sci U S A 1996 : On the other hand, three tumor derived mutant forms of p53 ( mut 143, mut 248, and mut 273 ) stimulated the activity of the IGF-I-R promoter and increased the levels of IGF-I-R/luciferase fusion mRNA
Ohlsson et al., Endocrinology 1998 (Osteosarcoma) : p53 regulates insulin-like growth factor-I (IGF-I) receptor expression and IGF-I induced tyrosine phosphorylation in an osteosarcoma cell line : interaction between p53 and Sp1 ... The aim of the present study was to investigate whether the IGF-IR is a physiological target for p53 in osteosarcoma cells ... The p53 induced regulation of IGF-IR levels was studied in a tetracycline regulated expression system ... When expressed in Saos-2, osteosarcoma cells that lack p53, wild-type p53 decreased, whereas mutated p53 increased IGF-IR expression, and IGF-I induced tyrosine phosphorylation of the IGF-IR ... However, Sp1 counteracted the inhibitory effect of p53 on IGF-IR promoter activity in a dose dependent manner ... In conclusion, p53 regulates IGF-IR expression, as reflected by a reduction in IGF-IR protein and a parallel reduction in IGF-I induced tyrosine phosphorylation of the IGF-IR and IRS-1 in an osteosarcoma cell line
Cianfarani et al., Eur J Clin Invest 1998 (Chromosome Fragility) : In vitro effects of growth hormone (GH) and insulin-like growth factor I and II ( IGF-I and -II ) on chromosome fragility and p53 protein expression in human lymphocytes ... IGF-I and -II also stimulate p53 protein expression that, taking part in DNA repair, may counteract the IGF action on genome stability
Wang et al., Biochem Biophys Res Commun 1998 : IGF I induction of p53 requires activation of MAP kinase in cardiac muscle cells ... The aim of this study was to investigate whether IGF I induction of p53 expression and p21 promoter require activation of MAP kinase in cardiac muscle cells ... These data indicate that transcriptional activation of p53 and p21WAF1/CIP1 by IGF I involves MAP kinase pathway in cardiomyocytes, and thus link MAP kinase to negative modulation of the cell cycle in cardiac muscle cells