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Potential action of IGF-1 and EGF on androgen receptor nuclear transfer and transactivation in normal and cancer human prostate cell lines.

Abstract：

:This work was designed to determine whether IGF-1 and EGF modulate nuclear transfer and transactivation of the androgen receptor (AR) in human prostate cell lines (PNT1A and DU-145). We first characterized the IGF-1 and EGF receptors by ligand-binding assays with [125I] IGF-1 and [125I] EGF in a normal human prostate epithelial cell line, PNT1A. We then evaluated the effects of these growth factors on AR nuclear transfer and transcriptional activation in this cell line and in DU-145, a human prostate tumor cell line. The cell lines were cotransfected with an AR expression vector and an androgen-responsive luciferase gene driven by the mouse mammary tumor virus (MMTV-luciferase) promoter. Neither IGF-1 nor EGF could activate reporter gene in the absence of androgens. Conversely, both enhanced the magnitude of the AR response in the presence of low levels of androgen (10(-11)-10(-9) M) and this response, increased by twofold, was inhibited by hydroxyflutamide. No effect of IGF-1 and EGF was observed on the intracellular localization of the fusion protein EGFP-AR in either cell line. The fluorescence stayed cytoplasmic even after 24 h of IGF-1 or EGF treatment. Taken together, these data indicate that growth factors are unable to initiate the nuclear translocation of AR in the absence of androgens or to induce ligand-independent transcriptional activity. We observed only cross-talk in the presence of androgens and IGF-1 or EGF, leading to an over-activated AR. In conclusion, the cross-talk between AR and growth factor signaling pathways may sensitize AR to suboptimal stimulation by low levels of androgens.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Orio F Jr,Térouanne B,Georget V,Lumbroso S,Avances C,Siatka C,Sultan C

doi

10.1016/s0303-7207(02)00374-x

keywords:

subject

Has Abstract

pub_date

2002-12-30 00:00:00

pages

105-14

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S030372070200374X

journal_volume

198

pub_type

杂志文章

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