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MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN.

Authors :
He, Tingting
Sun, Yifei
Zhang, Yingchun
Zhao, Shigang
Zheng, Yanjun
Hao, Guimin
Shi, Yuhua
Source :
Reproductive Biology & Endocrinology. 8/17/2019, Vol. 17 Issue 1, pN.PAG-N.PAG. 1p.
Publication Year :
2019

Abstract

Background: Polycystic ovary syndrome (PCOS) is one of the most common endocrine metabolic disorders characterized by hyperandrogenism, polycystic ovaries and ovulatory dysfunction. Several studies have reported that the aberrant expression of miRNAs contributes a lot to disordered folliculogenesis in PCOS, though the role and underlying mechanism of microRNA-200b (miR-200b) and microRNA-200c (miR-200c) in the development of PCOS remain unclear. Methods: The expression of miR-200b in granulosa cells (GCs) derived from 90 PCOS patients and 70 controls was analyzed by using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Granulosa-like tumor cell line (KGN) was cultured for cell counting kit-8 (CCK-8) assays after over-expression of miR-200b, miR-200c or knockdown phosphatase and tensin homolog (PTEN). TargetScan was used to identify the potential targets of miR-200b and miR-200c, which was further verified by qRT-PCR, western blot and luciferase assays. Results: Significantly increased expression of miR-200b was observed in PCOS patients compared with the controls. Moreover, over-expression of miR-200b and miR-200c inhibited the proliferation of KGN cells. In addition, our results verified that miR-200b and miR-200c directly targeted PTEN, knockdown of which suppressed KGN cells proliferation. Conclusion: Our findings demonstrate that miR-200b and miR-200c suppress the proliferation of KGN cells by targeting PTEN, and this might provide new evidence for abnormal proliferation of GCs in PCOS. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
14777827
Volume :
17
Issue :
1
Database :
Academic Search Index
Journal :
Reproductive Biology & Endocrinology
Publication Type :
Academic Journal
Accession number :
138126635
Full Text :
https://doi.org/10.1186/s12958-019-0505-8