.png){kind=icon}
.png){kind=icon}
Return
miR-191-5p Is Involved in Polycystic Ovary Syndrome by Targeting SOX4
.png){kind=icon}
PRE
AI
J
Y
S
J
R
L
W
DOI：10.1002/jbt.70974.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Polycystic ovary syndrome (PCOS) is a common refractory reproductive endocrine disorder in women. It is urgent to identify reliable biomarkers and explore the underlying molecular mechanisms of PCOS pathogenesis. A total of 199 subjects were enrolled in this study, including 108 PCOS patients and 91 healthy people. MiR-191-5p expression and diagnostic value were evaluated utilizing RT-qPCR and the ROC curve. Chi-square test was utilized to assess the correlation between baseline characteristics and miR-191-5p level in PCOS patients. The target gene of miR-191-5p was predicted by the TargetScan database. The correlation between miR-191-5p and SOX4 in PCOS was analyzed using Pearson's correlation. In KGN cells, miR-191-5p and SOX4 were overexpressed or inhibited using Lipofectamine 3000. Factors related to ferroptosis and proliferation were detected by CCK-8 assay, ferroptosis-related factors kits, and RT-qPCR. miR-191-5p was downregulated in PCOS and presented good diagnostic efficiency. miR-191-5p is closely related to baseline characteristics of PCOS and serves as a risk factor for PCOS. In KGN cells, overexpression of miR-191-5p promoted proliferation and suppressed ferroptosis, while inhibition of miR-191-5p reduced proliferation and increased ferroptosis. In PCOS, SOX4 was identified as a downstream target of miR-191-5p and was negatively regulated by miR-191-5p. In KGN cells, overexpression of SOX4 reduced proliferation and increased ferroptosis. miR‑191‑5p is aberrantly expressed in PCOS and may serve as a potential diagnostic biomarker. miR‑191‑5p participates in the progression of PCOS by negatively regulating SOX4 and modulating cell proliferation and ferroptosis.
Keywords:
ferroptosis
miR-191-5p
polycystic ovary syndrome
proliferation
SOX4
Journal
IF:
2.8
Papers:
3.7K
Citations:
5.9K
Organization
Cited Papers