Linked Life Data

17875736

Source:http://linkedlifedata.com/resource/pubmed/id/17875736

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2007-9-18
pubmed:abstractText
Prostate carcinomas frequently express estrogen receptors (ER), irrespective of androgen receptor (AR) expression; however, the role of ERs and estrogens in prostate cancer is controversial. We found that 17beta-estradiol (E(2)) is able to markedly up-regulate insulin-like growth factor (IGF)-I receptor (IGF-IR) mRNA and protein expression in both AR-positive (LNCaP cells) and AR-negative (PC-3 cells) prostate cancer cells. This effect occurs not only via ERalpha but also via ERbeta stimulation and is specific for IGF-IR because it does not involve the cognate insulin receptor. IGF-IR up-regulation is associated with increased IGF-IR phosphorylation and with increased mitogenic and motogenic activities in response to IGF-I. IGF-IR up-regulation by E(2) does not require ER binding to DNA and is poorly sensitive to antiestrogen blockade, whereas it is associated with the activation of cytosolic kinase cascades involving Src, extracellular signal-regulated kinase (ERK)-1/2, and, to a lesser extent, phosphatidylinositol 3-kinase and is sensitive to the inhibition of these kinases. In conclusion, our data indicate that estrogens may contribute to IGF system deregulation in prostate cancer through the activation of a nongenotropic pathway. Estrogens may have a role, therefore, in tumor progression to androgen independence. Inhibition of the IGF-IR or the Src-ERK pathway should be considered, therefore, as an adjuvant therapy in prostate cancer.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
67
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8932-41
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17875736-Cell Line, Tumor, pubmed-meshheading:17875736-Estradiol, pubmed-meshheading:17875736-Estrogen Receptor alpha, pubmed-meshheading:17875736-Estrogen Receptor beta, pubmed-meshheading:17875736-Humans, pubmed-meshheading:17875736-MAP Kinase Signaling System, pubmed-meshheading:17875736-Male, pubmed-meshheading:17875736-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:17875736-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:17875736-Phosphorylation, pubmed-meshheading:17875736-Promoter Regions, Genetic, pubmed-meshheading:17875736-Prostatic Neoplasms, pubmed-meshheading:17875736-RNA, Messenger, pubmed-meshheading:17875736-Receptors, Somatomedin, pubmed-meshheading:17875736-Transfection, pubmed-meshheading:17875736-Up-Regulation, pubmed-meshheading:17875736-src-Family Kinases
pubmed:year
2007
pubmed:articleTitle
17beta-estradiol up-regulates the insulin-like growth factor receptor through a nongenotropic pathway in prostate cancer cells.
pubmed:affiliation
Endocrinologia, Dipartimento di Medicina Interna e Medicina Specialistica, University of Catania, Ospedale Garibaldi-Nesima, Catania, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't