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MiR-23a induced the activation of CDC42/PAK1 pathway and cell cycle arrest in human cov434 cells by targeting FGD4

Ji Lin1,2,3, Huijuan Huang2, Liheng Lin4

  • 1Graduate School, Fujian Medical University, Fuzhou, China.

Journal of Ovarian Research
|August 11, 2020
PubMed
Abstract

Insights

MicroRNA-23a (miR-23a) downregulation is linked to Polycystic Ovary Syndrome (PCOS). MiR-23a regulates cell proliferation and apoptosis via FGD4, impacting PCOS pathophysiology.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) are crucial in ovarian function, including follicular development and ovulation.
  • Dysregulation of miRNAs is implicated in ovarian cancer and polycystic ovary syndrome (PCOS).

Purpose of the Study:

  • To investigate the specific role of microRNA-23a (miR-23a) in human granulosa-like cells (cov434).
  • To explore the potential involvement of miR-23a in the pathophysiology of PCOS.

Main Methods:

  • Analysis of miR-23a levels in PCOS patients' serum.
  • In vitro studies using miR-23a mimic and inhibitor in cov434 cells.
  • Cell proliferation assays, apoptosis assays, flow cytometry for cell cycle analysis.
  • Double luciferase reporter assay to confirm direct targeting of FGD4.
  • Western blotting to assess CDC42 and PAK1 activation.

Main Results:

  • Serum miR-23a was downregulated in PCOS patients and correlated with BMI, LH, Testosterone, Glucose, and Insulin.
  • miR-23a mimic inhibited cov434 cell proliferation and induced apoptosis, arresting the cell cycle at G0/G1 phase.
  • miR-23a directly targets FGD4, suppressing its expression.
  • miR-23a activation of CDC42/PAK1 pathway mediates cell cycle arrest.

Conclusions:

  • miR-23a regulates proliferation and apoptosis in cov434 cells by targeting FGD4.
  • miR-23a plays a significant role in the pathophysiology of PCOS.
Keywords:
Binding siteCell cycleFGD4Polycystic ovary syndromemiR-23a

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