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Tibolone Effects on Human Glioblastoma Cell Lines

Aliesha González-Arenas1, Marisol De la Fuente-Granada1, Ignacio Camacho-Arroyo2

  • 1Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad Universitaria, Ciudad de México, México.

Archives of Medical Research
|September 10, 2019
PubMed
Abstract

Insights

Tibolone (TIB) increases glioblastoma cell proliferation by affecting estrogen and progesterone receptors. This study investigated TIB

Area of Science:

  • Neuro-oncology
  • Endocrinology
  • Cell Biology

Background:

  • Glioblastoma (GBM) growth is modulated by ovarian steroid hormones via intracellular receptors.
  • Activation of sex hormone receptors contributes to glioblastoma progression.
  • Tibolone (TIB), a selective estrogenic activity regulator, has unknown effects on glioblastoma.

Purpose of the Study:

  • To evaluate TIB's effects on glioblastoma cell number, migration, and invasion.
  • To determine TIB's role in estrogen receptor (ER) and progesterone receptor (PR) activity and content.

Main Methods:

  • Human glioblastoma cell lines (U251-MG, U87) were treated with varying doses of TIB.
  • Cell proliferation, migration, and invasion assays were performed.
  • Protein expression of ERs and PRs was analyzed using Western blot.

Main Results:

  • TIB (10 nM) significantly increased glioblastoma cell proliferation without affecting migration or invasion.
  • TIB-induced proliferation was inhibited by ER and PR antagonists (ICI 182,780 and RU 486).
  • TIB altered ER and PR content, increasing ER-α, ER-β, and PR-B, while decreasing PR-A.

Conclusions:

  • Tibolone enhances glioblastoma cell proliferation via ER and PR modulation.
  • ER and PR signaling pathways are implicated in TIB's proliferative effects on glioblastoma cells.
  • TIB influences the expression levels of specific ER and PR isoforms.
Keywords:
Estrogen receptorHuman glioblastomaProgesterone receptorTiboloneU251-MG cellsU87 cells

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