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首页> 外文期刊>Journal of cellular physiology. >Hypermethylation-mediated down regulation of lncRNA PVT1 promotes granulosa cell apoptosis in premature ovarian insufficiency via interacting with Foxo3a
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Hypermethylation-mediated down regulation of lncRNA PVT1 promotes granulosa cell apoptosis in premature ovarian insufficiency via interacting with Foxo3a

机译：Hypermethylation-mediated下来的监管lncRNA PVT1促进颗粒细胞凋亡通过交互过早卵巢机能不全与Foxo3a

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Long noncoding RNA PVT1 is involved in the progression of female gynecological cancers. However, the role of PVT1 in ovarian granulosa cell apoptosis-mediated premature ovarian insufficiency (POI) remains unclear. This study aims to elucidate the role of PVT1 in ovarian granulosa cell apoptosis-mediated POI. The expression of PVT1 was compared between ovarian tissues from POI patients and normal controls. The methylation level in the PVT1 promoter region was detected by methylation-specific polymerase chain reaction. The interaction between PVT1 and forkhead box class O3A (Foxo3a) was confirmed by RNA pull-down and RNA immunoprecipitation assays. Granulosa cell apoptosis was detected using flow cytometry. The effect of PVT1 on transcription activity of Foxo3a was detected by luciferase reporter assay. The expression of PVT1 was low in the POI ovarian tissues compared with the controls, and such a low expression was related to the hypermethylation of the PVT1 promoter. PVT1 was localized in both the cytoplasm and the nucleus of granulosa cells. We determined that PVT1 could bind with Foxo3a and that downregulating PVT1 by small interfering RNAs inhibited Foxo3a phosphorylation by promoting SCP4-mediated Foxo3a dephosphorylation, resulting in an increase in Foxo3a transcription activity. Moreover, downregulating PVT1 promoted granulosa cell apoptosis by increasing the Foxo3a protein levels. An in vivo experiment showed that the injection of PVT1 overexpressing vectors restored the ovarian function in POI mice. Hypermethylation-induced downregulation of PVT1 promotes granulosa cell apoptosis in POI by inhibiting Foxo3a phosphorylation and increases the Foxo3a transcription activity.
机译：长非编码RNA PVT1参与发展的女性妇科癌症。然而,PVT1在卵巢颗粒的作用细胞apoptosis-mediated过早卵巢不足(POI)仍不清楚。旨在阐明PVT1在卵巢的作用颗粒细胞apoptosis-mediated POI。表达PVT1卵巢之间的比较组织从POI患者和正常对照组。PVT1启动子区域的甲基化水平是被methylation-specific聚合酶连锁反应。forkhead框类O3A (Foxo3a)证实了下拉和RNA RNA免疫沉淀反应化验。使用流颗粒细胞凋亡检测血细胞计数。Foxo3a活动被荧光素酶检测记者分析。POI的卵巢组织相比控制和如此低的表达有关PVT1启动子的甲基化。PVT1在细胞质和本地化颗粒细胞的细胞核。PVT1可以用Foxo3a,绑定表达下调PVT1小干扰rna抑制Foxo3a磷酸化通过促进SCP4-mediated Foxo3a去磷酸化,产生的Foxo3a转录活动的增加。此外,表达下调PVT1促进了颗粒细胞凋亡增加Foxo3a蛋白质的水平。注入PVT1 overexpressing向量恢复POI老鼠的卵巢功能。的差别Hypermethylation-induced对这些PVT1POI的促进颗粒细胞凋亡Foxo3a磷酸化,抑制增长Foxo3a转录活动。

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