| http://purl.uniprot.org/citations/18451178 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18451178 | http://www.w3.org/2000/01/rdf-schema#comment | "Insulin-like growth factor-I (IGF-I) is a polypeptide hormone that can influence growth, differentiation, and survival of cells expressing the cognate type 1 receptor (IGF-IR). To better understand cell autonomous IGF-IR signaling in the epithelial compartment of the prostate gland, we generated a conditional (Cre/loxP) prostate-specific IGF-IR knockout mouse model. In contrast to epidemiologic studies that established a correlation between elevated serum IGF-I and the risk of developing prostate cancer, we show that abrogation of IGF-IR expression in the dorsal and lateral prostate could activate extracellular signal-regulated kinase 1/2 signaling and cause cell autonomous proliferation and hyperplasia. Moreover, persistent loss of IGF-IR expression in dorsal and ventral lobes induced p53-regulated apoptosis and cellular senescence rescue programs, predicting that titration of IGF-IR signaling might facilitate growth of tumors with compromised p53 activity. Therefore, we crossed the mice carrying the prostate-specific IGF-IR knockout alleles into the transgenic adenocarcinoma of the mouse prostate model that is driven, in part, by T antigen-mediated functional inactivation of p53. Consistent with our prediction, prostate epithelial-specific deletion of IGF-IR accelerated the emergence of aggressive prostate cancer when p53 activity was compromised. Collectively, these data support a critical role for IGF-IR signaling in prostate tumorigenesis and identify an important IGF-IR-dependent growth control mechanism."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-07-6531"xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/author | "Wang F."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/author | "Greenberg N.M."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/author | "Knoblaugh S.E."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/author | "Sutherland B.W."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/author | "Holzenberger M."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/author | "Kaplan-Lefko P.J."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/pages | "3495-3504"xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/title | "Conditional deletion of insulin-like growth factor-I receptor in prostate epithelium."xsd:string |
| http://purl.uniprot.org/citations/18451178 | http://purl.uniprot.org/core/volume | "68"xsd:string |
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