Effect of Methylation Status of lncRNA-MALAT1 and MicroRNA-146a on Pulmonary Function and Expression Level of COX2 in Patients With Chronic Obstructive Pulmonary Disease

Abstract

This study aimed to investigate the role of methylation of MALAT1 and miR-146a in the pathogenesis of chronic obstructive pulmonary disease (COPD). COPD patients were grouped according to their methylation status of MALAT1 and miR-146a promoters, and we found that forced vital capacity, volume that has been exhaled at the end of the first second of forced expiration, and diffusion capacity for carbon monoxide were the highest in the MALAT1 HYPO + miR-146a HYPER group and lowest in the MALAT1 HYPER + miR-146a HYPO group, and COPD patients with hypermethylated MALAT1 showed lower expression of MALAT1 than that in the COPD patients with hypomethylated MALAT1. Meanwhile, miR-146a was the most significantly upregulated in the MALAT1 HYPER + miR-146a HYPO group and the most significantly downregulated in the MALAT1 HYPO + miR-146a HYPER group. Both prostaglandin E1 and cyclooxygenase 2 (COX2) expression were the highest in the MALAT1 HYPO + miR-146a HYPER group and the lowest in the MALAT1 HYPER + miR-146a HYPO group. In conclusion, our results established a MALAT1/miR-146a/COX2 signaling axis. The overexpression of MALAT1 could increase the expression of COX2 by inhibiting the expression of miR-146a, thus affecting the pulmonary function of COPD patients.

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

“…As far as we know, lncRNA can inhibit the expression of miRNA to regulate gene expression and regulate physiological and pathological processes. 26 In our investigation, based on bioinformatics analysis, miR-212-5p was screened and verified to bind with LINC00599 in 16HBE cells. As an important member of the miR family, miR-212-5p has been reported to be dysregulated in a variety of human diseases, such as non-alcoholic fatty liver disease, 27 nasopharyngeal carcinoma, 28 and ovarian cancer.…”

Identification of Ferroptosis-Related Hub Genes and Their Association with Immune Infiltration in Chronic Obstructive Pulmonary Disease by Bioinformatics Analysis

“…The hsa-let-7b-5p participated in endothelial mitochondrial dynamics and acted as a biomarker for diagnosing Parkinsonian Syndromes. 32 , 33 The hsa-miR-1-3p inhibited lung adenocarcinoma cell tumorigenesis and improved gefitinib resistance in EGFR mutant lung cancer cell. 34 , 35 Additionally, the upstream lncRNAs of two miRNAs were predicted using ENCORI database and we found six lncRNAs with the most experimental evidence.…”

Focus on long non-coding RNA MALAT1: Insights into acute and chronic lung diseases

“…In TGF-β-treated HFL-1 cells, repressing MALAT1 boosts cell proliferation and suppresses the expression of fibronectin and α-SMA (Hu et al, 2020). Another study revealed that overexpressed MALAT1 elevates cyclooxygenase two expression via inhibiting miR-146a, which can affect pulmonary functions in COPD patients (Sun et al, 2021). Liu et al indicated that high expression of MALAT1 can be served as a biomarker to predict the acute exacerbation risk and disease conditions in COPD patients (Liu et al, 2020).…”