Hsa_circ_0043533 modulates apoptosis and viability of granulosa cells via miR-409-3p/BCL2 and EMT signalling in PCOS: providing a novel perspective of metformin

Author:

Ma Jing1,Liu Chang2,Zhang Huimin3,Zhao Mingzi1,Zhu Wenqian4,Du Xin3,Hao Cuifang3

Affiliation:

1. Qingdao University

2. Shanghai Jiao Tong University

3. Qingdao Woman and Children’s Hospital

4. Binzhou Medical University

Abstract

Abstract PCOS (polycystic ovary syndrome) is an important cause of infertility in women of child birthing age. It was confirmed granulosa cells were associated closely with the process of anomalous follicle formation and ovulation in PCOS. The apoptosis of granulosa cells in PCOS patients is significantly low but the growth is high, which cause accumulation granulosa cells, leading to polycystic ovaries. Non-coding RNAs was demonstrated involving in PCOS, and we found high hsa_circ_0043533 in PCOS. A series of experiments were carried out to investigate the role of hsa_circ_0043533 in PCOS and the mechanism within. Knockdown of hsa_circ_0043533 promoted apoptosis and restrained migration, proliferation, and viability of KGN cells. The regulation of hsa_circ_0043533 on miR-409-3p/BCL2 axis and key EMT (Epithelial-mesenchymal transition) markers was discovered. And the hsa_circ_0043533/miR-409-3p/BCL2 axis was regulated by metformin. This project revealed novel insights into the molecular mechanisms of granulosa cell proliferation and apoptosis in PCOS, demonstrated the new molecular pathogenesis of PCOS.

Publisher

Research Square Platform LLC

Reference33 articles.

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3. Franks S, McCarthy MI, Hardy K (2006) Development of polycystic ovary syndrome: involvement of genetic and environmental factors. Int J Androl 29, 278–285; discussion 286–290

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