ArticleJournal of ovarian research2020
MiR-23a induced the activation of CDC42/PAK1 pathway and cell cycle arrest in human cov434 cells by targeting FGD4.
Article in Journal of ovarian research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Gene regulatory activity associated with polycystic ovary syndrome revealed DENND1A-dependent testosterone production.Nature communications · 2025Article
- Circulating Cell Free microRNAs in Women with Polycystic Ovary Syndrome: Advancing Towards Biomarker Discovery and Therapeutic Targets.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- MicroRNAs as Biomarkers for Metabolic Disorders in Polycystic Ovary Syndrome (PCOS): A Review.Medical science monitor : international medical journal of experimental and clinical research · 2024Review
- Multi-omics insights and therapeutic implications in polycystic ovary syndrome: a review.Functional & integrative genomics · 2023Review
- p21-activated kinase 1 (PAK1) as a therapeutic target for cardiotoxicity.Archives of toxicology · 2022Review
- A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Atorvastatin reduces IOP in ocular hypertensionInternational journal of molecular medicine · 2022Article
- Advances in the study of CDC42 in the female reproductive system.Journal of cellular and molecular medicine · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMiRNAs play important roles in the development of ovarian cancer, activation of primitive follicles, follicular development, oocyte maturation and ovulation. In the present study, we investigated the specific role of miR-23a in cov434 cells.
resultsDownregulation of miR-23a was observed in serum of PCOS patients compared with the healthy control, suggesting the inhibitory effect of miR-23a in PCOS. MiR-23a was positively correlated with Body Mass Index (BMI) and negatively correlated with Luteinizing hormone (LH), Testostrone (T), Glucose (Glu) and Insulin (INS) of PCOS patients. MiR-23a mimic inhibited the proliferation and promoted apoptosis of human cov434 cells. In addition, flow cytometry assay confirmed that miR-23a blocked cell cycle on G0/G1 phase. MiR-23a inhibitor showed opposite results. Furthermore, double luciferase reporter assay proved that miR-23a could bind to the 3'UTR of FGD4 directly through sites predicted on Target Scan. FGD4 level was significantly suppressed by miR-23a mimic, but was significantly enhanced by miR-23a inhibitor. We further proved that miR-23a increased the expression of activated CDC42 (GTP bround) and p-PAK-1, suggesting that miR-23a induced cell cycle arrest through CDC42/PAK1 pathway.
conclusionsIn conclusion, our study reveals that miR-23a participates in the regulation of proliferation and apoptosis of cov434 cells through target FGD4, and may play a role in the pathophysiology of PCOS.
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