Evaluation of frizzled class receptor 3 and miR-378 expression levels in cumulus cells of polycystic ovary syndrome women: A case-control study

TL;DR

This study investigates how FZD3 and miR-378 gene expression in cumulus cells affects oocyte maturation in women with PCOS.

Contribution

The study reports novel expression patterns of FZD3 and miR-378 in cumulus cells of immature versus mature oocytes in PCOS patients.

Findings

FZD3 and miR-378 are overexpressed in cumulus cells of immature oocytes in PCOS women.

High FZD3 and miR-378 levels may inhibit oocyte maturation by disrupting WNT signaling and gene regulation.

Abstract

Polycystic ovarian syndrome (PCOS) is a common endocrine disorder that affects women of reproductive age. Recent studies suggest that frizzled class receptor 3 (FZD3) and miR-378 play significant roles in PCOS by affecting oocyte maturation.

Considering the importance of FZD3 and miR-378 in ovulation, the present study aimed to determine the expression levels of FZD3 and miR-378 genes in cumulus cells of germinal vesicles and metaphase II oocytes in women with PCOS.

The samples for this case-control study included, randomly selected, 25 women with PCOS who were treated at the Research and Clinical Center for Infertility, Yazd, Iran. The diagnosis of PCOS was made based on the criteria defined in the Rotterdam guidelines. Quantitative real-time polymerase chain reaction determined the expression level of FZD3 and miR-378.

This study showed increased expression of FZD3 and miR-378 in cumulus cells of immature oocytes compared to mature oocytes (p
<
0.0001).

High levels of FZD3 and miR-378 in cumulus cells of immature oocytes can inhibit their maturation. FZD3, a component of the WNT signaling pathway, is overexpressed in immature oocytes and may negatively affect the maturation process. Additionally, miR-378 inhibits oocyte development by targeting and repressing essential genes. Currently, various aspects of microRNA function remain unknown. MiR-378 may exert its regulatory role by directly targeting the FZD3 gene or by targeting other genes and mediators that interact with FZD3 or the protein it encodes. This study may provide a foundation for further investigation of this hypothesis in future research.

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