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Doxorubicin induces cytotoxicity and miR-132 expression in granulosa cells.
Metadata
Journalreproductive toxicology3.121Date
2020 Jun 04
4 months ago
Type
Journal Article
Volume
2020-Jun-04 / 96 : 95-101
Author
Al-Kawlani B 1, Murrieta-Coxca JM 1, Chaiwangyen W 2, Fröhlich K 1, Fritzsche A 3, Winkler S 3, Markert UR 4, Morales-Prieto DM 1
Affiliation
  • 2. Placenta Lab, Department of Obstetrics, Jena University Hospital, Jena, Germany; Department of Biochemistry, School of Medical Sciences, University of Phayao, Phayao, Thailand.
  • 3. Infertility Center Jena, Jena, Germany.
  • 4. Placenta Lab, Department of Obstetrics, Jena University Hospital, Jena, Germany. Electronic address: [email protected]
Doi
PMIDMESH
Abstract
Doxorubicin (DOX) is one of the most commonly used drugs for the treatment of childhood cancers, including leukemia and lymphomas. Despite the high survival rate, female leukemia survivors are at higher risk of ovarian failure and infertility later in life. Treatment with chemotherapeutic drugs like DOX is associated with damage in ovarian follicles, but the affectation grade of granulosa cells remains unclear. To assess and avoid the possible side-effects of DOX, early biomarkers of ovarian injury and chemotherapy-induced ovarian toxicity should be identified. MicroRNAs (miRNAs) have emerged in recent years as a promising new class of biomarkers for drug-induced tissue toxicity. In this study, the effects of DOX on cell viability, steroidogenesis, and miRNA expression were studied in primary granulosa cells (GCs) and in two cellular models (COV434 and KGN cells). We report that compared to other chemotherapeutic drugs, DOX treatment is more detrimental to granulosa cells as observed by decrease of cell viability. Treatment with DOX changes the expression of the aromatase gene (CYP19A1) and the secretion of 17β-estradiol (E2) in a cell-specific manner. miR-132-3p is dose-dependently increased by DOX in all cellular models. In absence of DOX, miR-132-3p overexpression in COV434 cells has no effect on E2 secretion or CYP19A1 expression. Altogether, these findings contribute to understanding the hormonal disbalance caused by DOX in human ovarian cells and suggest miR-132 as a putative sensor to predict DOX-induced ovarian toxicity.
Keywords: Doxorubicin Granulosa cells Ovarian toxicity miR-132 miRNAs
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Reprod Toxicolreproductive toxicology
Metadata
LocationUnited States
FromPERGAMON-ELSEVIER SCIENCE LTD

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