JME
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Journal of Molecular Endocrinology (2005) 35, 191-199    DOI: 10.1677/jme.1.01704
© 2005 Society for Endocrinology

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Roger, C
Right arrow Articles by Fenichel, P
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roger, C
Right arrow Articles by Fenichel, P

Estrogen-induced growth inhibition of human seminoma cells expressing estrogen receptor ß and aromatase

C Roger, S Lambard1, A Bouskine, B Mograbi, D Chevallier, M Nebout, G Pointis, S Carreau1 and P Fenichel

INSERM U 670, 28 avenue de Valombrose, Faculté de Médecine, 06102 Nice Cedex 2, France
1 UPRES EA 2608-USC INRA, Université-IBFA, Caen 14032, France

(Requests for offprints should be addressed to P Fenichel; Email: Fenichel{at}unice.fr)

It is now well established that estrogens participate in the control of normal spermatogenesis and endogenous or environmental estrogens are involved in pathological germ cell proliferation including testicular germ cell tumors. Studying a human testicular seminoma cell line, JKT-1, we show here that 17ß-estradiol (10–12 to 10–6 M) induced in vitro a significant dose-dependent decrease of cell growth. This antiproliferative effect was maximum after 4 days of exposure at a physiologically intratesticular concentration of 10–9 M, close to the Kd of ER, and reversed by ICI 182780, an ER antagonist, suggesting an ER-mediated pathway. By RT-PCR and Western blot we were able to confirm that JKT-1, like tumoral seminoma cells and normal human testicular basal germ cells, expresses estrogen receptor ß (ERß), including ERß1 and ERß2, a dominant negative variant, but not ER{alpha}. Using immunofluorescence and confocal microscopy, ERß was observed as perinuclear intracytoplasmic spots in JKT-1 and tumoral seminoma cells without significant translocation of ERß into the nucleus, under 17ß-estradiol exposure. Double staining observed by confocal microscopy revealed that ERß colocalized in JKT-1 cells with cytochrome C, a mitochondrial marker. We report for the first time the expression of a functional aromatase complex in seminoma cells as assessed by RT-PCR, Western blot and enzymatic assay. Seminoma cells are able to respond to estrogens through a possible autocrine or paracrine loop. These preliminary results support estrogen-dependency of human testicular seminoma, the most frequent tumor of young men, and suggest potential pharmacological use. Whether this estrogen control, however, involves an ERß-mediated stimulation of cell apoptosis and/or an ERß-mediated inhibition of cell proliferation, remains to be further determined.




This article has been cited by other articles:


Home page
EndocrinologyHome page
A. Bouskine, M. Nebout, B. Mograbi, F. Brucker-Davis, C. Roger, and P. Fenichel
Estrogens Promote Human Testicular Germ Cell Cancer through a Membrane-Mediated Activation of Extracellular Regulated Kinase and Protein Kinase A
Endocrinology, February 1, 2008; 149(2): 565 - 573.
[Abstract] [Full Text] [PDF]


Home page
Biol. Reprod.Home page
T. F.G Lucas, E. R Siu, C. A Esteves, H. P Monteiro, C. A Oliveira, C. S Porto, and M. F. M Lazari
17Beta-Estradiol Induces the Translocation of the Estrogen Receptors ESR1 and ESR2 to the Cell Membrane, MAPK3/1 Phosphorylation and Proliferation of Cultured Immature Rat Sertoli Cells
Biol Reprod, January 1, 2008; 78(1): 101 - 114.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the Society for Endocrinology.