Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieChronic Obstructive Pulmonary Disease
CeRNA1MEG3[LncRNA]
miRNAmiR-181a-2-3p[miRNA]
CeRNA2NA[mRNA]
Tissue/Cell line16HBE cells
SpecieHomo sapiens (human)
CitationOncol Lett. 2021 Jan;21(1):45. doi: 10.3892/ol.2020.12306. Epub 2020 Nov 17.
Reference title
Long non-coding maternally expressed gene 3 regulates cigarette smoke extract-induced apoptosis, inflammation and cytotoxicity by sponging miR-181a-2-3p in 16HBE cells.
Experimental verification
Dual-luciferase reporter assay;ELISA;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;
Functional description
Accumulating evidence has suggested that long non-coding (lnc)RNAs are widely involved in the progression of multiple diseases, including chronic obstructive pulmonary disease (COPD). The aim of the present study was to explore the function and molecule mechanism of maternally expressed gene 3 (MEG3) in cigarette smoke extract (CSE)-treated 16HBE cells. Cell viability and apoptosis were evaluated using Cell Counting Kit-8 analysis and flow cytometry, respectively. Western blot analysis was carried out to determine the protein levels of Bcl-2, Bax and cleaved caspase-3. ELISA assays were utilized to measure the protein levels of IL-1β and IL-6 and TNF-α. Cytotoxicity was assessed using a lactate dehydrogenase release assay. The expression levels of MEG3 and microRNA (miR)-181a-2-3p were detected using reverse transcription-quantitative PCR. The interaction between miR-181a-2-3p and MEG3 was predicted using DIANA tools and verified by a dual-luciferase reporter assay and RNA Immunoprecipitation assay. MEG3 expression was enhanced while miR-181a-2-3p abundance was reduced in the serum of patients with COPD and CSE-treated 16HBE cells. MEG3-knockdown or miR-181a-2-3p-overexpression inhibited CSE-induced apoptosis, inflammation and cytotoxicity in 16HBE cells. Moreover, miR-181a-2-3p directly bind to MEG3 and its knockdown reversed the inhibitory effect of MEG3 interference on apoptosis, inflammation and cytotoxicity in CSE-treated 16HBE cells. Overall, MEG3-knockdown suppressed CSE-induced apoptosis, inflammation and cytotoxicity in 16HBE cells by upregulating miR-181a-2-3p, providing a promising therapeutic target for treatment of CSE-induced COPD.
Annotations
External Annotation for MEG3 |
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LncRNA-associated competing triplets and functions. |
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Comprehensive experimentally supported associations between lncRNA and human cancer. |
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Infer genomic variations that disturb lncRNA-associated ceRNA regulation.. |
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Provide and annotate disease or phenotype-associated variants in human long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) or their regulatory elements. |
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Providing cellular-specific lncRNA-associated ceRNA networks predicted via high-throughput analysis of single-cell genomic data. |
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Information on all annotated and predicted human genes. |
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Gene nomenclature, gene families and associated resources (genomic, proteomic, phenotypic information). |
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Genome browser for vertebrate genomes. |
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An annotated collection of all publicly available DNA sequences. |
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A wiki-based platform for community curation of human long non-coding RNAs. |
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An integrated knowledge database dedicated to non-coding RNAs. |
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An integrated database of human annotated lncRNA transcripts. |
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Comprehensive annotations of eukaryotic long non-coding RNAs. |
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Comprehensive experimentally supported associations between lncRNA and human cancer. |
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A comprehensive, authoritative compendium of human genes and genetic phenotypes. |
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The catalogue of somatic mutations in cancer. |
