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

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.

Molecular characterization of extracellular vesicles derived from follicular fluid of women with and without PCOS: integrating analysis of differential miRNAs and proteins reveals vital molecules involving in PCOS

“…It should be also addressed that recent research found that downregulation of miR-206 can promote the human granulosa-like tumor cell line, KGN cells, proliferation, inhibit cell apoptosis, and further promote the development of PCOS [ 54 , 55 ]. Jiang et al found that high expression of miR-204 can improve insulin resistance (IR) of PCOS via the inactivation of TLR4/NF-κB pathway [ 56 ].…”

Whispers of the polycystic ovary syndrome theater: Directing role of long noncoding RNAs

“…The receiver operating characteristic curve demonstrated that lncROR could be a diagnostic marker for PCOS, with an AUC of 0.893. Inhibition of the lncROR/miR-206/vascular endothelial growth factor pathway led to decreased cell proliferation and increased cell apoptosis [ 74 ]. Most discussed lncRNAs, which are associated with GC function and hormone dysregulation, are also overexpressed in patients with PCOS rather when compared with that in controls, and further research is needed to verify the predictor characteristics.…”

“… [ 40 ] [ 41 ] KGN cells ROR (regulator of reprogramming) Up Down regulation of lncROR/miR-206/VEGF pathway inhibited cell proliferation and promoted cell apoptosis. [ 74 ] Human ovarian, KGN cells SNHG7(small nucleolar RNA host gene 7) / miR-21 downregulated SNHG7, then the proliferation of KGN cells was prevented and apoptosis was induced in GCs. [ 45 ] Endometrium of PCOS rats SNHG20 (small nucleolar RNA host gene 20) Up Metformin exhibited a therapeutic effect in the treatment of EH by modulating the lncRNA-MEG3/miR-223/GLUT4 and lncRNA-SNHG20/miR-4486/GLUT4 signaling pathways.…”