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Journal of Endocrinology (2004) 183, 69-78       DOI: 10.1677/joe.1.05696
© 2004 Society for Endocrinology
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Hormonal regulation of H19 gene expression in prostate epithelial cells

N Berteaux, S Lottin, E Adriaenssens, F Van Coppenolle1, X Leroy2, J Coll3, T Dugimont4 and J-J Curgy

Unité INSERM ESPRI: Signalisation des facteurs de croissance dans le cancer du sein, Protéomique fonctionnelle, Université des Sciences et Technologies de Lille, 59655 Villeneuve d’Ascq cedex, France
1 Laboratoire de Physiologie cellulaire, INSERM EPI-9938, Université des Sciences et Technologies de Lille, 59655 Villeneuve d’Ascq, France
2 Laboratoire d’Anatomie et Cytologie pathologiques, Hôpital Huriez, Pôle Recherche, Faculté de Médecine, 1 Place de Verdun, Centre Hospitalier Universitaire, 59045 Lille cedex, France
3 Immunopathologie cellulaire des maladies infectieuses, CNRS UMR 8527, Institut de Biologie Moléculaire, Institut Pasteur, 1 Rue Calmette, 59019 Lille cedex, France
4 Faculté des Sciences Jean Perrin, Université d’Artois, 62307 Lens cedex, France

(Requests for offprints should be addressed to J-J Curgy; Email curgy{at}univ-lille1.fr)

The H19 gene is transcribed in an mRNA-like noncoding RNA. When tumors of various organs or cell types are considered, H19 oncogene or tumor-suppressor status remains controversial. To address the potential regulation of H19 gene expression by an androgen steroid hormone (DHT: dihydrotestosterone) or by a peptidic hormone (PRL: prolactin), we performed experiments in rats systemically treated with chemical mediators. This range of in vivo experiments demonstrated that chronic hyperprol-actinemia upregulated the H19 expression in epithelial and stromal cells whereas DHT downregulated the gene. PRL and DHT appeared to be opposite mediators in the H19 RNA synthesis. We investigated these hormonal effects in three human prostate epithelial cell lines. In LNCaP cancer cells, the opposite effect of PRL and DHT was corroborated. However, in normal cells (PNT1A), H19 remained insensitive to the hormones in fetal calf serum (FCS) medium but became responsive in a serum-stripped medium. In the DU-145 cancer cell line, tested for its androgen-independence and aggressiveness, the hormones had no effect on H19 expression whatever the culture conditions. Finally, we demonstrated that PRL upregulated the H19 expression in LNCaP cells by the JAK2–STAT5 transduction pathway. We conclude that H19 expression is regulated by both a peptidic and a male steroid hormone.







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