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Mechanisms of regulation of cell adhesion and motility by insulin receptor substrate-1 in prostate cancer cells
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Mechanisms of regulation of cell adhesion and motility by insulin receptor substrate-1 in prostate cancer cells
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Journal Article
Mechanisms of regulation of cell adhesion and motility by insulin receptor substrate-1 in prostate cancer cells
2001
Overview
LNCaP cells are human prostatic cancer cells that have a frame-shift mutation of the tumor suppressor gene PTEN and do not express the insulin receptor substrate-1 (IRS-1), a major substrate of the type 1 insulin-like growth factor receptor (IGF-IR). Ectopic expression of IRS-1 in LNCaP cells increases cell adhesion and decreases cell motility by an IGF-I-independent mechanism. We show now that these effects of IRS-1 are accompanied by serine phosphorylation of IRS-1 and are inhibited by inhibitors of phosphatidylinositol 3-kinase (PI3K). We have confirmed the requirement for PI3K activity and serine phosphorylation by the use of IRS-1 mutants, expressed in LNCaP cells. Serine phosphorylation inhibits IGF-I-induced tyrosyl phosphorylation of IRS-1, which is restored by the expression of wild-type PTEN or by inhibition of PI3K activity. Finally, IRS-1 in LNCaP cells co-immunoprecipitates with integrin alpha 5 beta 1, and the association is again IGF-I-independent. We conclude that in LNCaP cells, IRS-1 is serine phosphorylated by PI3K, generating effects that are different, and even opposite, from those generated by IGF-I.
Publisher
Nature Publishing,Nature Publishing Group
Subject
/ Adenocarcinoma - physiopathology
/ Biological and medical sciences
/ Biology
/ Cell Adhesion - drug effects
/ Fundamental and applied biological sciences. Psychology
/ Humans
/ Insulin
/ Insulin Receptor Substrate Proteins
/ insulin receptor substrate-1
/ Kinases
/ Male
/ Molecular and cellular biology
/ Motility
/ Mutation
/ Phosphatidylinositol 3-Kinases - antagonists & inhibitors
/ Phosphoproteins - metabolism
/ Prostatic Neoplasms - pathology
/ Prostatic Neoplasms - physiopathology
/ Prostatic Neoplasms - secondary
