Progesterone inhibits Pit-1 and prolactin gene expression but activates promoter activity of c-H-Ras oncogene in the rat pituitary adenoma GH3 cell

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Journal Article

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Molecules and Cells






The present study examined the effects of estrogen (E) and progesterone (P) on the proLactin (PRL), and Pit-1 gene expression and ras promoter activity in the GH3 cell. GH3 cells were incubated with 17β-estradiol (E) or vehicle (V). Two days later, progesterone (P) was supplemented in the culture medium. Four experimental groups were examined: vehicle (VV), P treatment alone (VP), E treatment alone (EV), and E and P treatment (EP). The results showed that E increased mRNA levels of PRL and Pit-1, while P suppressed the E-dependent induction of PRL and Pit-1 mRNA levels. To investigate the effect of E and P on ras promoter activity, the c-H-ras promoter conjugated with the β-galactosidase coding region was transfected into GH3 cells and the promoter activity was detected by enzyme linked immunosorbent assay (ELISA) for β-galactosidase. Administration of E or P alone had no effect on ras promoter activity and the proliferation of GH3 cells, while addition of P to E-primed conditions significantly enhanced ras promoter activity as well as proliferation of GH3 cells. These data indicate that P inhibits gene expression of Pit-1 and PRL, but activates ras promoter activity under E-primed conditions, respectively. Therefore, Pit-1 seemed to be involved in the regulation of prolactin synthesis by P, while the signaling pathway of ras might be correlated inversely to the regulation of PRL synthesis by P. © 1996 The Korean Society for Molecular Biology.

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