Estetrol Increases Progesterone Genetic Response without Triggering Common Estrogenic Effects in Endometriotic Cell Lines and Primary Cultures

Author:

Patiño-García Daniel12ORCID,Palomino Jaime3ORCID,Pomés Cristián2,Celle Claudia2,Torres-Estay Verónica14,Orellana Renán15ORCID

Affiliation:

1. Departamento de Ciencias Químicas y Biológicas, Facultad de Ciencias de la Salud, Universidad Bernardo O’Higgins, General Gana 1702, Santiago 8370874, Chile

2. División de Ginecología, Escuela de Medicina, Pontificia Universidad Católica de Chile, Alameda 340, Santiago 8331150, Chile

3. Escuela de Medicina Veterinaria, Facultad de Ciencias Médicas, Universidad Bernardo O’Higgins, General Gana 1702, Santiago 8370874, Chile

4. Escuela de Química y Farmacia, Facultad de Medicina y Ciencia, Universidad San Sebastián, Bellavista 7, Santiago 8420524, Chile

5. Programa de Magíster en Ciencias Químico Biológicas, Facultad de Ciencias de la Salud, Universidad Bernardo O’Higgins, General Gana 1702, Santiago 8370874, Chile

Abstract

Estetrol (E4), a natural estrogen produced by the human fetal liver, is actively studied for menopause and breast cancer treatment. It has low side effects and preferential estrogen receptor alpha (ERα) affinity. There are no data about its effects on endometriosis, a common gynecological disease affecting 6–10% of cycling women, generating painful pelvic lesions and infertility. Current combined hormone treatment (progestins and estrogens) is safe and efficient; nevertheless, one-third of patients develop progesterone (P4) resistance and recurrence by reducing P4 receptors (PRs) levels. We aimed to compare E4 and 17β-estradiol (E2) effects using two human endometriotic cell lines (epithelial 11Z and stromal Hs832 cells) and primary cultures from endometriotic patients. We evaluated cell growth (MTS), migration (wound assay), hormone receptors levels (Western blot), and P4 response by PCR array. Compared to E2, E4 did not affect cell growth or migration but increased estrogen receptor alpha (ERα) and PRs, and reduced ERβ. Finally, the incubation with E4 improved the P4 gene response. In conclusion, E4 increased PRs levels and genetic response without inducing cell growth or migration. These results suggest that E4 might be useful for endometriosis treatment avoiding P4 resistance; however, evaluating its response in more complex models is required.

Funder

The National Fund for Scientific and Technological Development

Publisher

MDPI AG

Subject

General Biochemistry, Genetics and Molecular Biology,Medicine (miscellaneous)

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