Abstract
The action of progestins is derived from many factors:structure, affinity for the progesterone receptor or for othersteroid receptors, the target tissue considered, the biologicalresponse, the experimental conditions, the dose andmetabolic transformation. The proliferative response toprogestins in human breast cancer cells is contradictory:some progestins inhibit, others stimulate, have no effectat all, or have a dual action. For instance,medroxyprogesterone acetate has a stimulatory effecton breast cancer cells after a short period of treatment,but this effect becomes inhibitory when treatmentis prolonged. It has been demonstrated that, inhormone-dependent breast cancer cells, various progestins(nomegestrol acetate, medrogestone, promegestone) arepotent sulfatase inhibitory agents. The progestins canalso involve the inhibition of the mRNA expression ofthis enzyme. In another series of studies it was also demonstratedthat some progestins are very active in inhibiting17β-hydroxysteroid dehydrogenase for the conversionof estrone to estradiol. More recently it was observed thatthe progestins promegestone and medrogestone stimulatesulfotransferase for the formation of estrogen sulfates.Consequently, the action of progestins in blockingestradiol formation via sulfatase, or in stimulating theeffect on sulfotransferase activity, can open interestingand new possibilities in clinical applications in breastcancer.
Published Version
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