Wang Huixiang, Ni Chengxiang, Xiao Wei, Wang Sulin
Department of Gynecology and Obstetrics, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Ann Transl Med. 2020 Nov;8(22):1504. doi: 10.21037/atm-20-6810.
Studies have considered long non-coding RNA 5 prime to Xist (lncRNA FTX) a key lncRNA for normal uterine development, but it has not been reported whether lncRNA FTX is involved in regulating the development of endometriosis (EMs). The aim of the present study was to explore the effect and mechanism of long non-coding RNA 5 prime to Xist (lncRNA FTX) on the invasion, metastasis, and epithelial-mesenchymal transition (EMT) of endometrial stromal cells (ESCs) caused by EMs.
Ectopic or normal endometrial tissues were collected from 38 patients with EMs, who were diagnosed and operated on at Beijing Tongren Hospital from June 2018 to December 2019, and 20 healthy volunteers with normal endometria. The expression of lncRNA FTX in both groups was detected by quantitative reverse transcription polymerase chain reaction. Ectopic endometrial stromal cells (EESC) and ESC from patients with EMs and healthy volunteers were separated and cultured, and the expression of lncRNA FTX in the cells was detected. The expression of lncRNA FTX in EESC was overexpressed or interfered. Proliferation, invasion, and migration was detected by Cell Counting Kit-8, transwell assay, and scratch assay. Apoptosis and cell cycle were detected by flow cytometry. EMT-related protein and PI3K/Akt signaling pathway-related protein expressions were detected by Western blot.
LncRNA FTX was underexpressed in endometrial tissues and EESC from patients with EMs. The overexpression of lncRNA FTX could significantly inhibit the proliferation, invasion, and migration of EESC, but promoted apoptosis and cell cycle arrest in the G0/G1 phase. The overexpression of lncRNA FTX significantly increased the expression of EMT-related protein, E-cadherin, and decreased the protein expression of vimentin, N-cadherin, and zinc finger E-box binding homeobox 1. In addition, the overexpression of lncRNA FTX could decrease the expression of p-PI3K/PI3K and p-Akt/Akt. Interfering with the expression of lncRNA FTX had the opposite result.
The overexpression of lncRNA FTX could decrease the invasion, metastasis, and EMT of ESC caused by EMs by inhibiting the activity of the PI3K/Akt signaling pathway.
研究认为长链非编码RNA 5端至Xist（lncRNA FTX）是正常子宫发育的关键lncRNA，但lncRNA FTX是否参与子宫内膜异位症（EMs）的发生发展尚未见报道。本研究旨在探讨lncRNA FTX对EMs所致子宫内膜基质细胞（ESCs）侵袭、转移及上皮-间质转化（EMT）的影响及机制。
收集2018年6月至2019年12月在北京同仁医院诊断并手术的38例EMs患者的异位或正常子宫内膜组织，以及20例子宫内膜正常的健康志愿者的组织。采用定量逆转录聚合酶链反应检测两组中lncRNA FTX的表达。分离培养EMs患者和健康志愿者的异位子宫内膜基质细胞（EESC）和ESCs，并检测细胞中lncRNA FTX的表达。对EESC中lncRNA FTX的表达进行过表达或干扰。采用细胞计数试剂盒-8、Transwell实验和划痕实验检测细胞增殖、侵袭和迁移能力。采用流式细胞术检测细胞凋亡和细胞周期。采用蛋白质免疫印迹法检测EMT相关蛋白和PI3K/Akt信号通路相关蛋白的表达。
lncRNA FTX在EMs患者的子宫内膜组织和EESC中表达下调。lncRNA FTX过表达可显著抑制EESC的增殖、侵袭和迁移，但促进细胞凋亡并使细胞周期阻滞于G0/G1期。lncRNA FTX过表达显著增加EMT相关蛋白E-钙黏蛋白的表达，降低波形蛋白、N-钙黏蛋白和锌指E盒结合同源框1的蛋白表达。此外，lncRNA FTX过表达可降低p-PI3K/PI3K和p-Akt/Akt的表达。干扰lncRNA FTX的表达则产生相反的结果。
lncRNA FTX过表达可通过抑制PI3K/Akt信号通路的活性，降低EMs所致ESCs的侵袭、转移及EMT。
