Abstract
The physiological effects of glucocorticoids (GCs) are, at least in part, mediated by inhibition of cell proliferation. Two isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) interconvert cortisol (F) and inactive cortisone (E), and are thus able to modulate GC action at an autocrine level. Previously, we have demonstrated absent expression of 11beta-HSD2 in normal pituitaries; however, in a small number of pituitary tumors analysed, 11beta-HSD2 was readily demonstrable. Here we have used real-time RT-PCR to quantify expression of mRNA for 11beta-HSD1 and 2 in 105 human pituitary tumors and have performed enzyme expression and activity studies in primary pituitary cultures. Overall, pituitary tumors expressed lower levels of 11beta-HSD1 mRNA compared with normals (0.2-fold, P
Original language | English |
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Pages (from-to) | 1663-1667 |
Number of pages | 5 |
Journal | Oncogene |
Volume | 22(11) |
Issue number | 11 |
Publication status | Published - 20 Mar 2003 |
Keywords
- proliferation
- 11 beta-hydroxysteroid dehydrogenase
- pituitary adenoma