RRC ID |
68122
|
著者 |
Li Y, Liu YD, Zhou XY, Zhang J, Wu XM, Yang YZ, Chen YX, Zhang XF, Li X, Ma LZ, Wang Z, Chen SL.
|
タイトル |
Let-7e modulates the proliferation and the autophagy of human granulosa cells by suppressing p21 signaling pathway in polycystic ovary syndrome without hyperandrogenism.
|
ジャーナル |
Mol Cell Endocrinol
|
Abstract |
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder in reproductive-aged women, and its pathogenesis is still under debate. Recent studies suggest crucial roles for microRNAs (miRNAs) in PCOS development. The let-7 family miRNAs constitute the most abundant miRNAs in human granulosa cells (GCs), and plays an important role in follicular development. However, research on the let-7e implications of the non-hyperandrogenic (non-HA) phenotype remains unclear. This study aimed at determining the role of let-7e in the progression of PCOS. We performed quantitative real-time PCR to examine the levels of let-7e in fifty-two non-HA PCOS patients and fifty-two controls. A receiver operating characteristic (ROC) curve were used to reveal the diagnostic value of let-7e in non-HA PCOS. Using an immortalized human granulosa cell line, KGN, we investigated the influence of let-7e on cell proliferation and autophagy. Our data substantiated the expression of let-7e was significantly increased in non-HA PCOS group, and associated with an increased antral follicle count. The ROC curve indicated a major separation between non-HA PCOS group and the control group. Let-7e knockdown suppressed cell proliferation and enhanced cell autophagy by activating p21 pathway. Conversely, let-7e overexpression promoted cell proliferation and inhibited cell autophagy by suppressing p21 pathway. Our results indicate that increased let-7e levels in non-HA PCOS GCs may contribute to excessive follicular activation and growth, thereby involving in the pathogenesis of PCOS. Let-7e may thus be a potential therapeutic target in non-HA PCOS.
|
巻・号 |
535
|
ページ |
111392
|
公開日 |
2021-9-15
|
DOI |
10.1016/j.mce.2021.111392
|
PII |
S0303-7207(21)00236-7
|
PMID |
34246727
|
MeSH |
Adult
Autophagy
Case-Control Studies
Cell Line
Cell Proliferation
Cyclin-Dependent Kinase Inhibitor p21 / genetics*
Female
Granulosa Cells / cytology*
Granulosa Cells / metabolism
Humans
Hyperandrogenism / genetics*
MicroRNAs / genetics*
Polycystic Ovary Syndrome / genetics*
Signal Transduction
Up-Regulation
|
IF |
3.871
|
リソース情報 |
ヒト・動物細胞 |
KGN(RCB1154) |