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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.

Hormonal regulation of H19 gene expression in prostate epithelial cells