首页|lncRNA作为ceRNA在多囊卵巢综合征中的作用

lncRNA作为ceRNA在多囊卵巢综合征中的作用

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多囊卵巢综合征(polycystic ovary syndrome,PCOS)是一种常见的女性生殖内分泌疾病,受表观遗传和环境等多种因素影响。长链非编码RNA(long non-coding RNA,lncRNA)为不编码蛋白质且长度超过200个核苷酸的RNA分子,其可通过表观遗传修饰、转录及转录后调控等影响基因的表达。lncRNA可作为竞争性内源RNA(competing endogenous RNA,ceRNA)与微小RNA(microRNA,miRNA)竞争性结合,从而调控靶基因表达。作为一种新的调控机制,其可在细胞增殖分化、炎症反应及免疫应答等生物过程中发挥重要作用,并且与许多疾病密切相关。ceRNA假说的提出也使学者们对PCOS的发生发展机制有了进一步了解。近年来,ceRNA在PCOS中的研究也越来越多。在PCOS中差异表达的lncRNA可作为ceRNA调控靶基因进而影响卵巢颗粒细胞增殖、卵母细胞成熟以及激素合成,这对PCOS的发生发展起到重要作用。综述lncRNA作为ceRNA在PCOS发生发展中的作用。
The Role of LncRNA as CeRNA in Polycystic Ovary Syndrome
Polycystic ovary syndrome(PCOS)is a common female reproductive endocrine disorder that is related with various factors including epigenetic and environment.Long non-coding RNA(lncRNA),with more than 200 nucleotides,are a kind of RNA molecules that do not code proteins.LncRNA can affect the expression of gene through epigenetic modification,transcriptional and post-transcriptional regulation.As a kind of competing endogenous RNA(ceRNA),lncRNA can affect the expression of target gene by competitively binding microRNA(miRNA).As a new regulatory mechanism,it can play an important role in many biological processes such as cell proliferation and differentiation,inflammatory response and immune response,which is closely related to many diseases.The ceRNA hypothesis also provides a further understanding of the mechanism of PCOS.Recently,the studies of lncRNA in PCOS significantly increased.The lncRNA differentially expressed in PCOS can involve as ceRNA in ovarian granulosa cell proliferation,oocyte maturation as well as hormone synthesis,and play an potential role in the development of PCOS.In this review,we summarize the roles of lncRNA as ceRNA in the occurrence and development of PCOS.

Polycystic ovary syndromeRNA,long noncodingCompeting endogenous RNAGene expressionOvary

代鹤琦、毛菲、冯睿芝、钱云

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210028 南京医科大学第二附属医院生殖医学中心

南京医科大学生殖医学与子代健康全国重点实验室

多囊卵巢综合征 RNA,长链非编码 竞争性内源RNA 基因表达 卵巢

2024

国际生殖健康/计划生育杂志
天津市医学科学技术信息研究所

国际生殖健康/计划生育杂志

CSTPCD
影响因子:0.694
ISSN:1674-1889
年,卷(期):2024.43(2)
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