Yang Zuwei, Pan Jiexue, Zhou Chengliang, Yu Chuanjin, Zhou Zhiyang, Ding Guolian, Liu Xinmei, Sheng Jianzhong, Jin Li, Huang Hefeng
Obstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China.
The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
iScience. 2023 Nov 23;27(2):108522. doi: 10.1016/j.isci.2023.108522. eCollection 2024 Feb 16.
Small nucleolar RNA host genes (SNHGs) have been implicated in various biological processes, yet their involvement in polycystic ovary syndrome (PCOS) remains elusive. Specifically, SNHG5, a long non-coding RNA implicated in several human cancers, shows elevated expression in granulosa cells (GCs) of PCOS women and induces PCOS-like features when overexpressed in mice. , SNHG5 inhibits GC proliferation and induces apoptosis and cell-cycle arrest at G0/G1 phase, with RNA-seq indicating its impact on DNA replication and repair pathways. Mechanistically, SNHG5 acts as a competing endogenous RNA by binding to miR-92a-3p, leading to increased expression of target gene , which further suppresses GC proliferation and promotes apoptosis. These findings elucidate the crucial role of SNHG5 in the pathogenesis of PCOS and suggest a potential therapeutic target for this condition. Additional investigations such as large-scale clinical studies and functional assays are warranted to validate and expand upon these findings.
小核仁RNA宿主基因（SNHGs）已被证明参与多种生物学过程，但其在多囊卵巢综合征（PCOS）中的作用仍不清楚。具体而言，SNHG5是一种与多种人类癌症相关的长链非编码RNA，在PCOS女性的颗粒细胞（GCs）中表达升高，在小鼠中过表达时会诱导PCOS样特征。此外，SNHG5抑制GC增殖，诱导细胞凋亡并使细胞周期停滞在G0/G1期，RNA测序表明其对DNA复制和修复途径有影响。机制上，SNHG5通过与miR-92a-3p结合作为竞争性内源性RNA，导致靶基因表达增加，进而进一步抑制GC增殖并促进细胞凋亡。这些发现阐明了SNHG5在PCOS发病机制中的关键作用，并提示了针对这种疾病的潜在治疗靶点。有必要进行更多的研究，如大规模临床研究和功能测定，以验证和扩展这些发现。
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