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微小 RNA-524-5p 通过靶向 Notch 信号通路中的 NUMB 调节 HTR-8/SVneo 滋养层细胞的增殖和侵袭。

MicroRNA‑524‑5p regulates the proliferation and invasion of HTR‑8/SVneo trophoblasts by targeting NUMB in the Notch signaling pathway.

机构信息

Department of Obstetrics, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, P.R. China.

出版信息

Mol Med Rep. 2021 Jun;23(6). doi: 10.3892/mmr.2021.12075. Epub 2021 Apr 13.

Abstract

Preeclampsia is a pregnancy disorder that is primarily associated with maternal and neonatal or fetal morbidity and mortality. The discovery of dysregulated microRNAs (miRs) and their roles in preeclampsia has provided new insight into the mechanisms involved in pregnancy‑related disorders. In the present study, quantitative PCR demonstrated that the expression levels of miR‑524‑5p were lower in patients with preeclampsia than those in normal pregnant women. Cell Counting Kit‑8 and Transwell assays indicated that overexpression of miR‑524‑5p promoted the proliferation and invasion of HTR‑8/SVneo cells, whereas inhibition of miR‑524‑5p suppressed HTR‑8/SVneo cell proliferation and invasion. Furthermore, NUMB endocytic adaptor protein (NUMB), a negative regulator of the Notch signaling pathway and a target gene of miR‑524‑5p, limited the effects of miR‑524‑5p on HTR‑8/SVneo cell invasion and migration. The present study demonstrated that miR‑524‑5p regulated the proliferation and invasion of HTR‑8/SVneo cells at least partly by targeting NUMB to regulate the Notch signaling pathway.

摘要

子痫前期是一种妊娠疾病,主要与母婴或胎儿发病率和死亡率相关。调控失常的 microRNAs(miRs)的发现及其在子痫前期中的作用为妊娠相关疾病的发生机制提供了新的见解。在本研究中,定量 PCR 显示,子痫前期患者 miR-524-5p 的表达水平低于正常孕妇。细胞计数试剂盒-8 和 Transwell 分析表明,miR-524-5p 的过表达促进了 HTR-8/SVneo 细胞的增殖和侵袭,而 miR-524-5p 的抑制则抑制了 HTR-8/SVneo 细胞的增殖和侵袭。此外,NUMB 内吞衔接蛋白(NUMB)是 Notch 信号通路的负调控因子,也是 miR-524-5p 的靶基因,限制了 miR-524-5p 对 HTR-8/SVneo 细胞侵袭和迁移的影响。本研究表明,miR-524-5p 通过靶向 NUMB 调节 Notch 信号通路来调节 HTR-8/SVneo 细胞的增殖和侵袭,至少部分是通过这种方式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f8b/8060792/dc6d1070fe6d/mmr-23-06-12075-g00.jpg

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