Journal
JOURNAL OF HUMAN GENETICS
Volume 66, Issue 2, Pages 123-137Publisher
SPRINGERNATURE
DOI: 10.1038/s10038-020-0819-6
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Funding
- Natural Science Foundation of Shanghai [19ZR1476100]
- National Infrastructures for Translational Medicine (Shanghai) [TMSK-2020-109]
- Interdisciplinary Program of Medical Engineering Cross Fund [YG2019GD02, YG2019QNB23, YG2019QNA49, YG2019QNA52]
- Laboratory Innovative Research Program of Shanghai Jiao Tong University [JCZXSJB2019002]
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The study revealed the crucial role of epigenetic interactions between miRNA and DNA methylation in the pathogenesis of polycystic ovarian syndrome (PCOS), with implications for gene expression regulation and potential molecular targets.
Aberration in microRNA expression or DNA methylation is a causal factor for polycystic ovarian syndrome. However, the epigenetic interactions between miRNA and DNA methylation remain unexplored in PCOS. We conducted a novel integrated analysis of RNA-seq, miRNA-seq, and methylated DNA-binding domain sequencing on ovarian granulosa cells to reveal the epigenetic interactions involved in the pathogenesis of PCOS. We identified 830 genes and 30 miRNAs that were expressed differently in PCOS, and seven miRNAs negatively regulated target mRNA expression. 130 miRNAs' promoters were significantly differently methylated, while 13 were associated with miRNA expression. Furthermore, the hypermethylation of miR-429, miR-141-3p, and miR-126-3p ' promoter was found related to miRNA expression suppression and therefore their corresponding genes upregulation, includingXIAP,BRD3,MAPK14,andSLC7A5. Our findings provide a novel insight in PCOS. The consequential reversal of genes silencing may participate in PCOS pathogenesis and served as potential molecular targets for PCOS.
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