Research Paper Volume 13, Issue 8 pp 11774—11785
Inhibition of sestrin 1 alleviates polycystic ovary syndrome by decreasing autophagy
- 1 Department of Obstetrics and Gynecology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China
- 2 Department of Cardiology, The First People's Hospital of Jingdezhen, Jingdezhen, Jiangxi 333000, China
- 3 Department of Cytogenetics Laboratory, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China
- 4 Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong 515041, China
Received: August 5, 2020 Accepted: February 27, 2021 Published: April 22, 2021https://doi.org/10.18632/aging.202872
How to Cite
Copyright: © 2021 Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, accounting for 50–70% of anovulatory infertility cases. However, the etiology of PCOS at the molecular level remains unclear. Here, bioinformatics analysis was performed to identify differentially expressed genes (DEGs) between adipose tissue of PCOS patients and matched tissues from non-hyperandrogenic women. RT-qPCR, western blot, cell counting kit-8 (CCK-8), EdU (5-Ethynyl-2'-deoxyuridine) staining, LC3 staining, ROS (reactive oxygen species) detection, and apoptosis assays were conducted to explore the effects of sestrin 1 on KGN human granulosa-like tumor cells. Bioinformatics analysis indicated that DEGs in adipose tissue from PCOS patients were enriched in the p53 signaling pathway. Moreover, sestrin 1 was identified as a major target of the p53 gene. Downregulation of sestrin 1 inhibited proliferation of KGN cells by inhibiting autophagy. Additionally, sestrin 1 downregulation increased ROS generation and promoted apoptosis in KGN cells. By contrast, overexpression of sestrin 1 increased cell viability by increasing autophagy in KGN cells. Together, these results suggest that downregulation of sestrin 1 may be a potential novel treatment strategy for PCOS.