Role of lncRNA FTX in invasion, metastasis, and epithelial-mesenchymal transition of endometrial stromal cells caused by endometriosis by regulating the PI3K/Akt signaling pathway
Background: 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. Methods: 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. Results: 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. Conclusions: 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.
第一作者机构：[1]Department of Gynecology and Obstetrics, Beijing Tongren Hospital, Capital Medical University, Beijing, China[*1]Department of Gynecology and Obstetrics, Beijing Tongren Hospital, Capital Medical University, Beijing, China
通讯作者：
通讯机构：[1]Department of Gynecology and Obstetrics, Beijing Tongren Hospital, Capital Medical University, Beijing, China[*1]Department of Gynecology and Obstetrics, Beijing Tongren Hospital, Capital Medical University, Beijing, China
推荐引用方式(GB/T 7714)：
Wang Huixiang,Ni Chengxiang,Xiao Wei,et al.Role of lncRNA FTX in invasion, metastasis, and epithelial-mesenchymal transition of endometrial stromal cells caused by endometriosis by regulating the PI3K/Akt signaling pathway[J].ANNALS OF TRANSLATIONAL MEDICINE.2020,8(22):doi:10.21037/atm-20-6810.
APA：
Wang, Huixiang,Ni, Chengxiang,Xiao, Wei&Wang, Sulin.(2020).Role of lncRNA FTX in invasion, metastasis, and epithelial-mesenchymal transition of endometrial stromal cells caused by endometriosis by regulating the PI3K/Akt signaling pathway.ANNALS OF TRANSLATIONAL MEDICINE,8,(22)
MLA：
Wang, Huixiang,et al."Role of lncRNA FTX in invasion, metastasis, and epithelial-mesenchymal transition of endometrial stromal cells caused by endometriosis by regulating the PI3K/Akt signaling pathway".ANNALS OF TRANSLATIONAL MEDICINE 8..22(2020)
