RU486-induced growth inhibition of human endometrial cells
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This study investigated the effects of RU486 on human endometrial cells and found that it inhibited their growth.
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Abstract
ObjectiveTo determine the direct action of RU486 on endometrial cell proliferation and to differentiate whether the antioxidant or the antiprogesterone property of RU486 is predominately responsible for its effect on cell growth.DesignIn vitro study comparing the effects of RU486 (antiprogesterone and antioxidant), reduced RU486 (antioxidant), ZK112,993 (antiprogesterone), and lazaroid U74,500A (antioxidant) on endometrial cell growth. The human endometrial cell line EM42 was used in transient transfection assays to confirm the relative antiprogesterone potency of the various compounds.SettingAcademic medical centerPatient(s)Women presenting with pelvic pain or infertility and diagnosed with endometriosis at time of surgery or women desiring tubal ligation with a normal pelvis (controls).Intervention(s)Endometrial cell cultures were treated with RU486, reduced RU486, lazaroid U74,500A, and ZK112,993.Main outcome measure(s)Tritiated thymidine incorporation was used to assess cell growth. Inhibition of progesterone induction of transiently transfected reporter plasmids was used to measure antiprogesterone activity of compounds studied.Result(s)RU486 reduced cell growth in a dose-dependent fashion of the endometrial cell lines EM42 and RL95-2 and of endometrial and endometriosis cells from primary culture. After being reduced, RU486 lost most of its antiprogesterone activity but retained its antiproliferative properties. ZK112,993 was similar in potency to RU486 as a progesterone antagonist but did not significantly modify endometrial cell growth. Lazaroid U74,500A was devoid of antiprogesterone activity but was shown to be a potent antiproliferative agent.Conclusion(s)RU486 has a direct inhibitory effect on human endometrial cell growth. This activity appears to be at least partly mediated through its antioxidant property.
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References (19)
- Endometrial effects of long-term low-dose administration of RU486 via openalex
- Evidence for Oxidatively Modified Lipid-Protein Complexes in Endometrium and Endometriosis via openalex
- Isolation, characterization, and comparison of human endometrial and endometriosis cells in vitro. via openalex
- doi:10.1016/s0303-7207(96)03980-9 via openalex
- W1603633107 via openalex
- doi:10.1152/physrev.1994.74.1.139 via openalex
- W2289519236 via openalex
- W6664125244 via openalex
- doi:10.1016/0010-7824(89)90004-8 via openalex
- doi:10.1016/s0015-0282(16)56659-x via openalex
- doi:10.1016/s0015-0282(16)53174-4 via openalex
- doi:10.1006/abbi.1993.1281 via openalex
- doi:10.1210/jcem-71-4-1074 via openalex
- doi:10.1016/0960-0760(95)00091-d via openalex
- doi:10.1016/0024-3205(91)90648-u via openalex
- doi:10.1016/s0002-9378(98)70316-3 via openalex
- doi:10.1016/s0022-5223(19)34627-6 via openalex
- doi:10.1172/jci117551 via openalex
- doi:10.1016/0304-3835(92)90023-o via openalex
Cited by (25)
- Investigation of the 12-month efficacy and safety of low-dose mifepristone in the treatment of painful adenomyosis 2022
- Physiology of the Endometrium and Regulation of Menstruation 2020
- Clinical analyses of endometriosis after conservative surgery. 2015
- Antiprogestins in gynecological diseases 2014
- Endometriosis and Oxidative Stress 2012
- Progesterone Resistance and Targeting the Progesterone Receptors: A Therapeutic Approach to Endometriosis 2012
- Clinical Aspects of Endometriosis 2010
- Constitutive and Tumor Necrosis Factor-Alpha-Stimulated Activation of Nuclear Factor-KappaB in Immortalized Endometriotic Cells and Their Suppression by Trichostatin A 2010
- Female Infertility and Antioxidants 2010
- Medical treatment of endometriosis. 2009
- Endometriosis causing lower extremity deep vein thrombosis — case report and review of the literature 2009
- Female Infertility and Free Radicals: Potential Role in Adhesions and Endometriosis 2006
- Nuclear Factor-κB (NF-κB): An Unsuspected Major Culprit in the Pathogenesis of Endometriosis That Is Still at Large? 2006
- Inhibition of Proliferation of Endometrial Stromal Cells by Trichostatin A, RU486, CDB-2914, N-Acetylcysteine, and ICI 182780 2006
- The role of progestins in treating the pain of endometriosis 2006
- Transcriptional Characterizations of Differences between Eutopic and Ectopic Endometrium 2005
- Future Perspectives in the Medical Treatment of Endometriosis 2005
- Novel targets for the treatment of endometriosis 2004
- Effects of oxidants and antioxidants on proliferation of endometrial stromal cells 2004
- Glucocorticoid receptor function suppresses insulin-like growth factor 1 activity in human KLE endometrial-like cells. 2004
- Medical Management of Endometriosis: Novel Targets and Approaches towards the Development of Future Treatment Regimes 2003
- Immunomodulators and aromatase inhibitors: are they the next generation of treatment for endometriosis? 2003
- Presence of endometrial epithelial cells in the peritoneal cavity and the mesothelial inflammatory response 2003
- Immunomodulators and aromatase inhibitors: are they the next generation of treatment for endometriosis? 2003
- Oxidative stress and peritoneal endometriosis 2002
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- europepmc
- last seen: 2026-07-27T06:15:28.040536+00:00
- openalex
- last seen: 2026-05-11T06:38:17.545654+00:00
- pubmed
- last seen: 2026-05-13T22:13:30.513821+00:00
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