Differential expression of long non-coding RNA Regulator of reprogramming and its molecular mechanisms in polycystic ovary syndrome

J Ovarian Res. 2021 Jun 21;14(1):79. doi: 10.1186/s13048-021-00829-6.

Abstract

Background: Polycystic ovary syndrome (PCOS) is a common endocrine disease in women of reproductive age. Multiple studies have shown that long non-coding RNAs (lncRNA) and microRNAs (miRNA) play a role in PCOS. This study aimed to explore the role and molecular mechanism of lncRNA -Regulator of reprogramming (lncROR) in PCOS.

Results: Expression level of lncROR in PCOS patients was up-regulated, while level of miR-206 was down-regulated in comparison with control group (P < 0.001). Logistics regression analysis showed that lncROR and miR-206 were independent predictors of PCOS. The ROC curve showed that lncROR had a high diagnostic value for PCOS with an AUC value of 0.893. Pearson correlation coefficient indicated that the expression level of miR-206 was negatively correlated with the level of lncROR. CCK-8 assay and apoptosis assay revealed that downregulation of lncROR up-regulated the expression of miR-206, thereby inhibiting cell proliferation and promoting cell apoptosis. However, silencing the expression of miR-206 reversed the above effects caused by down-regulation of lncROR expression. Luciferase reporter gene assay suggested that there was a target relationship between lncROR and miR-206. VEGF was proved to be the target gene of miR-206.

Conclusions: Highly expressed lncROR indirectly up-regulated the expression of VEGF by down-regulating the expression of miR-206, thereby promoting the proliferation of KGN cells and inhibiting apoptosis, and further promoting the development of PCOS.

Keywords: MiR-206; Polycystic ovary syndrome; Regulator of reprogramming; Vascular endothelial growth factor.

MeSH terms

  • Adult
  • Apoptosis
  • Cell Proliferation
  • Female
  • Humans
  • Polycystic Ovary Syndrome / genetics*
  • Polycystic Ovary Syndrome / pathology
  • RNA, Long Noncoding / metabolism*
  • Transfection

Substances

  • RNA, Long Noncoding