<p>LINC00987 Ameliorates COPD by Regulating LPS-Induced Cell Apoptosis, Oxidative Stress, Inflammation and Autophagy Through Let-7b-5p/SIRT1 Axis</p>

Abstract

Background: Chronic obstructive pulmonary disease (COPD) is the third cause of diseaserelated death and brings a heavy burden to human health. Long non-coding RNA (lncRNA) was revealed to participate in COPD pathogenesis. This study aims to establish the effects and regulatory mechanism of lncRNA long intergenic non-coding 00987 (LINC00987) in lipopolysaccharide (LPS)-induced apoptosis, oxidative stress, inflammation and autophagy in BEAS-2B cells. Methods: The expression levels of LINC00987 and let-7b-5p were detected by real-time quantitativepolymerase chain reaction (RT-qPCR). The expression of apoptosis-associated proteins, oxidative stress (ROS)-related proteins, autophagy-related proteins and sirtuin1 (SIRT1) protein was determined by Western blot. Cell viability was illustrated by cell counting kit-8 (CCK-8) assay. Cell apoptosis was investigated by caspase3 activity and apoptosis analysis assays. ROS, inflammation and autophagy were demonstrated by detecting reactive ROS level and superoxide dismutase (SOD) activity, enzyme-linked immunosorbent assay (ELISA) and Western blot analysis, respectively. The binding sites between let-7b-5p and LINC00987 or SIRT1 were predicted by lncBase or miRWalk online database, and identified by dual-luciferase reporter assay. Results: LINC00987 expression was strikingly downregulated and let-7b-5p expression was obviously upregulated in COPD tissues and LPS-induced BEAS-2B cells compared with control groups. LINC00987 overexpression promoted BEAS-2B cells against LPS-mediated viability, apoptosis, oxidative stress, inflammation and autophagy, whereas these effects were attenuated by let-7b-5p mimic or SIRT1 knockdown. Furthermore, LINC00987 sponged let-7b-5p and let-7b-5p bound to SIRT1. Conclusion: LINC00987 ameliorated COPD through modulating LPS-induced cell apoptosis, oxidative stress, inflammation and autophagy via sponging let-7b-5p to associate with SIRT1. This finding will provide a theoretical basis for the research of LncRNA-mediated treatment in COPD.

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

“…For example, COPDA1 promotes the proliferation of smooth muscle cells through upregulating the expression of MS4A1 in COPD ( Zheng et al, 2019 ). LINC00987 modulates LPS-induced cell apoptosis, oxidative stress, inflammation and autophagy through sponging let-7b-5p in COPD ( Wang et al, 2020 , Chen, Chen, Liu, Dong, Ji, Hu, Zhang). MEG3 targets miR-218 thereby regulating cigarette smoke extract (CSE)-inhibited proliferation and CSE-induced apoptosis in COPD ( Song et al, 2020 ).…”

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“…LINC00987 was transfected into LPS-induced 16HBE and BEAS-2B cells with a control group. LINC00987 protected 16HBE and BEAS-2B cells from LPS-induced apoptosis, oxidative stress, inflammation, and autophagy (Wang et al, 2020). In our research, LINC00987 upregulation was found to be deeply involved in immune system events.…”

Identification and validation of an epigenetically regulated long noncoding RNA model for breast cancer metabolism and prognosis

“…Among the 14 lncRNAs in MylnBrna, several lncRNAs have been well studied in several abnormal metabolic diseases and tumours. For instance, ensg00000237248 (LINC00987) has been reported to ameliorate chronic obstructive pulmonary disease through modulating lipopolysaccharide-induced cell apoptosis, oxidative stress, inflammation, and autophagy via regulating other gene signalling pathways [ 39 ]. The down-regulation of ensg00000232352 (lncRNA SEMA3B-AS1) was related to risky outcomes of patients with Wilms tumour [ 40 ].…”