MicroRNA-16 represses granulosa cell proliferation in polycystic ovarian syndrome through inhibition of the PI3K/Akt pathway by downregulation of Apelin13

Abstract

This study aimed to uncover the specific role of micro RNA-16 (miR-16) in granulosa cell function in polycystic ovarian syndrome (PCOS). After sample collection, the expression levels of miR-16 and Apelin13 in the granulosa cells of PCOS patients and controls were determined. Subsequently, miR-16 mimic, miR-16 inhibitor, pcDNA3.1-Apelin13, sh-Apelin13, and their corresponding negative controls were transfected into granulosa cell lines (KGN and SVOG) to monitor alterations in miR-16 expression, Apelin13, and PI3K/Akt signalling pathway-related proteins (p-Akt and Akt). MTT assay was used to detect cell viability, clone formation assay to detect cell proliferation, and flow cytometry to detect cell apoptosis rate. In addition, a luciferase assay was performed to test the targeting relationship between miR-16 and Apelin13. After miR-16 overexpression or Apelin13 knockdown was achieved in granulosa cells, granulosa cell proliferation was suppressed and cell apoptosis was enhanced. Additionally, Apelin13 is a potential target of miR-16. Functionally, overexpression of Apelin13 could partly reverse the effect of miR-16 overexpression on granulosa cell proliferation and apoptosis. Moreover, inhibits granulosa cell proliferation and enhances blocking the PI3K/Akt pathway by suppressing Apelin13. Our study revealed miR-16 regulates Apelin13 to mediate the PI3K/Akt signalling pathway and, thereby mediates PCOS progression.

Keywords:

• Polycystic ovarian syndrome
• granulosa cell
• MicroRNA-16
• Apelin13

Acknowledgment

Thanks for all the contributors.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This research was funded by the grant from Intra-Hospital Fund of the First Hospital of Lanzhou University [Grant No. ldyyyn2019-37].