Donglan Yuan1, Dandan Zhu1, Boyu Yin1, Hongshan Ge1, Yinling Zhao1, Aihua Huang1, Xiaosu Wang1, Xiuhong Cao2, Nan Xia1, Hua Qian3. 1. Department of Obstetrics and Gynecology, Taizhou People's Hospital Affiliated to Nantong University, 399 Hailing Road, Taizhou, 225300, People's Republic of China. 2. Department of Operation, Taizhou People's Hospital Affiliated to Nantong University, Taizhou, 225300, China. 3. Department of Obstetrics and Gynecology, Taizhou People's Hospital Affiliated to Nantong University, 399 Hailing Road, Taizhou, 225300, People's Republic of China. qh1526611@163.com.
Abstract
BACKGROUND: Endometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear. OBJECTIVE: This report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM. METHODS: Endometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays. RESULTS: MiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p. CONCLUSIONS: NEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression.
BACKGROUND: Endometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear. OBJECTIVE: This report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM. METHODS: Endometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays. RESULTS: MiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p. CONCLUSIONS: NEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression.
Authors: Diana Bautista-Sánchez; Cristian Arriaga-Canon; Abraham Pedroza-Torres; Inti Alberto De La Rosa-Velázquez; Rodrigo González-Barrios; Laura Contreras-Espinosa; Rogelio Montiel-Manríquez; Clementina Castro-Hernández; Verónica Fragoso-Ontiveros; Rosa María Álvarez-Gómez; Luis A Herrera Journal: Mol Ther Nucleic Acids Date: 2020-03-13 Impact factor: 8.886