Let-7e modulates the proliferation and the autophagy of human granulosa cells by suppressing p21 signaling pathway in polycystic ovary syndrome without hyperandrogenism
| Autor: | Yi-zhen Yang, Yu-Dong Liu, Xiao-Fei Zhang, Ying Li, Ying-Xue Chen, Zhe Wang, Xin Li, Jun Zhang, Xiao-min Wu, Shi-Ling Chen, Xing-Yu Zhou, Lin-zi Ma |
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| Rok vydání: | 2021 |
| Předmět: |
Adult
Cyclin-Dependent Kinase Inhibitor p21 endocrine system diseases Granulosa cell Cell Biology Biochemistry Cell Line Endocrinology microRNA medicine Autophagy Humans Molecular Biology Cell Proliferation Granulosa Cells Cell growth Polycystic ovary syndrome (PCOS) Hyperandrogenism medicine.disease Polycystic ovary Up-Regulation MicroRNAs medicine.anatomical_structure Case-Control Studies Cancer research Female Polycystic Ovary Syndrome Signal Transduction |
| Zdroj: | Molecular and cellular endocrinology. 535 |
| ISSN: | 1872-8057 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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