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The estrogen metabolites 2-methoxyestradiol and 2-hydroxyestradiol inhibit endometriotic cell proliferation in estrogen-receptor-independent manner.
Journal article

The estrogen metabolites 2-methoxyestradiol and 2-hydroxyestradiol inhibit endometriotic cell proliferation in estrogen-receptor-independent manner.

  • Samartzis EP a Division of Gynecology , University Hospital of Zurich , Zurich , Switzerland and.
  • Imesch P a Division of Gynecology , University Hospital of Zurich , Zurich , Switzerland and.
  • Twiehaus A b Clinic for Reproductive Endocrinology, University Hospital of Zurich , Zurich , Switzerland.
  • Dubey RK b Clinic for Reproductive Endocrinology, University Hospital of Zurich , Zurich , Switzerland.
  • Leeners B b Clinic for Reproductive Endocrinology, University Hospital of Zurich , Zurich , Switzerland.
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  • 2016-01-23
Published in:
  • Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. - 2016
2-hydroxyestradiol
2-methoxyestradiol
Endometriosis
estrogen metabolites
fulvestrant (ICI 182780)
2-Methoxyestradiol
Cell Line
Cell Proliferation
Dose-Response Relationship, Drug
Endometriosis
Estradiol
Estrogen Receptor Antagonists
Female
Fulvestrant
Humans
English Endometriosis, a painful disorder associated with infertility, is estimated to occur in approximately 7-10% of reproductive age women. Although endometriosis is considered as an estrogen-dependent disease, the role of estrogen metabolites via receptor-independent mechanisms has not yet been comprehensively clarified. In the present study, growth studies were performed comparing the effect of estradiol (E2), estrogen metabolites, that is, 2-hydroxyestradiol (2-OHE2) and 2-methoxyestradiol (2-ME), as well as estrogen-receptor-independent mechanisms using the estrogen receptor antagonist fulvestrant, on cell proliferation of endometriotic cells. The estrogen metabolites 2-OHE2 and 2-ME inhibited cell growth in a dose-dependent manner in pharmacological doses. Lower concentrations of 2-OHE2 had a stimulating effect on cell proliferation while pharmacologic doses exerted an antimitogenic effect. The effects on cell growth were at least partially receptor-independent, as demonstrated by simultaneous receptor antagonization with fulvestrant. In conclusion, our results demonstrate that in pharmacological doses the estrogen metabolites 2-ME and 2-OHE2 show inhibiting effects on the proliferation of endometriotic cells and may be promising substances for the treatment of endometriosis.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/296395
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