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Estrogen-induced growth inhibition of human seminoma cells expressing estrogen receptor β and aromatase
- Source :
- Journal of Molecular Endocrinology; May 2005, Vol. 35 Issue: 1 p191-199, 9p
- Publication Year :
- 2005
-
Abstract
- 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 17β-estradiol (10−12to 10−6M) induced in vitroa significant dose-dependent decrease of cell growth. This antiproliferative effect was maximum after 4 days of exposure at a physiologically intratesticular concentration of 10−9M, close to the Kdof 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 β (ERβ), including ERβ1 and ERβ2, a dominant negative variant, but not ERα. Using immunofluorescence and confocal microscopy, ERβ was observed as perinuclear intracytoplasmic spots in JKT-1 and tumoral seminoma cells without significant translocation of ERβ into the nucleus, under 17β-estradiol exposure. Double staining observed by confocal microscopy revealed that ERβ 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 ERβ-mediated stimulation of cell apoptosis and/or an ERβ-mediated inhibition of cell proliferation, remains to be further determined.
Details
- Language :
- English
- ISSN :
- 09525041 and 14796813
- Volume :
- 35
- Issue :
- 1
- Database :
- Supplemental Index
- Journal :
- Journal of Molecular Endocrinology
- Publication Type :
- Periodical
- Accession number :
- ejs8810121
- Full Text :
- https://doi.org/10.1677/jme.1.01704