NDLI: MicroRNA-93 promotes ovarian granulosa cells proliferation through targeting CDKN1A in polycystic ovarian syndrome.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Lin Chen, Yaxiao Zhao, Xiaomiao Jiang, Linlin Huang, Jia Chen, Xiaoli Yang, Dongzi
Description	Author Affiliation: Jiang L ( Department of Obstetrics and Gynecology (L.J., J.H., L.L., Y.C., X.C., X.Z., D.Y.), Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120 China.)
Abstract	CONTEXT: MicroRNAs (miRNAs) are small, noncoding RNAs that negatively regulate gene expression post-transcriptionally. Whether differently expressed miRNAs contribute to promoting granulosa cell proliferation in polycystic ovarian syndrome disease (PCOS) remains unknown. OBJECTIVE: We explored whether certain miRNAs are involved in the ovarian dysfunction of PCOS and the mechanism of increased granulosa cells proliferation. Patients and Cells: miRNA expression was analyzed in excised ovarian cortexes from 16 women with PCOS and 8 non-PCOS. An immortalized human granulosa (KGN) cell was used for the mechanism study. MAIN OUTCOME MEASURES: Expressions of miRNAs in ovarian cortexes were measured using qRT-PCR and KGN granulosa cells were cultured for proliferation assays after overexpression or inhibition of miR-93 or after insulin treatment. Bioinformatics were used to identify the potential miRNA targets. Protein expression analysis, luciferase assays, and rescue assays were used to confirm the substrate of miR-93. RESULTS: MiR-93 expression was higher in PCOS ovarian cortex and its identified target, CDKN1A, was downregulated. MiR-93 overexpression promoted cell proliferation and G1 to S transition. Knocking down CDKN1A promoted cell growth and cell cycle progression in granulosa cells, and CDKN1A re-introduction reversed the promotional role of miR-93. High concentrations of insulin induced upregulation of miR-93, stimulated KGN cells proliferation and reduced CDKN1A expression. CONCLUSIONS: miR-93 was increased in PCOS granulosa cells and targeted CDKN1A to promote proliferation and cell cycle progression. Insulin could upregulate the expression of miR-93 and stimulate cell proliferation. This might provide a new insight into the dysfunction of granulosa cells in PCOS.
ISSN	0021972X
e-ISSN	19457197
DOI	10.1210/jc.2014-3827
Journal	The Journal of Clinical Endocrinology & Metabolism
Issue Number	5
Volume Number	100
Language	English
Publisher	Oxford University Press
Publisher Date	2015-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Proliferation Genetics Cyclin-dependent Kinase Inhibitor P21 Metabolism Granulosa Cells Micrornas Polycystic Ovary Syndrome Cell Cycle Cell Line Down-regulation Cytology Research Support, Non-u.s. Gov't Discipline Endocrinology Discipline Metabolism
Content Type	Text
Resource Type	Article
Subject	Biochemistry (medical) Endocrinology, Diabetes and Metabolism Clinical Biochemistry Biochemistry Endocrinology

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