Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieAutoimmune Thyroiditis
CeRNA1MALAT1[LncRNA]
miRNAmiR-206[miRNA]
CeRNA2PTGS1[mRNA]
Tissue/Cell lineAIT tissues and Nthy-ori 3-1 cells
SpecieHomo sapiens (human)
CitationPsychopharmacology (Berl). 2021 Apr;238(4):1141-1156. doi: 10.1007/s00213-021-05761-7. Epub 2021 Jan 16.
Reference title
Ursolic acid ameliorates Nthy-ori 3-1 cells injury induced by IL-1β through limiting MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway.
Experimental verification
ELISA;Flow cytometry assay;Western blot;Flow Cytometry assay;luciferase assay;
Functional description
RATIONALE: Ursolic acid (UA) has exhibited anti-inflammatory and anti-oxidative drug effects. OBJECTIVES: In the research, we assessed the effects of UA on Nthy-ori 3-1 cells stimulated by IL-1β and attempted to elucidate the mechanisms underlying the effects. METHODS: Autoimmune thyroiditis (AIT) was simulated using Nthy-ori 3-1 cells by IL-1β (10 μM) treatment. UA (20 μM) was applied to ameliorate the injury of Nthy-ori 3-1 cells. The target of UA was predicted by TCMSP, BATMAN, and GEO database. Targeted relationship between lncRNA MALAT1 and miR-206, as well as miR-206 and PTGS1, was predicted by bioinformatics software and identified by dual luciferase assays. Cytokines in the cell supernatant and the apoptosis of cells were detected by ELISAs and flow cytometry assays, respectively. Expression levels of NF-κB signaling pathway-related proteins were estimated by western blot. RESULTS: By enquiring TCMSP, BATMAN, and GEO database, PTGS1 was identified as a target of UA. Afterward, a ceRNA network among MALAT1, miR-206, and PTGS1 was constructed. The expression levels of MALAT1 and PTGS1 in AIT tissues were obviously enhanced. Moreover, the ceRNA network formed by MALAT1/miR-206/PTGS1 contributed to the damage of Nthy-ori 3-1 cells induced by IL-1β. However, UA ameliorated the Nthy-ori 3-1 cells injury induced by IL-1β through mediating the MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway. CONCLUSIONS: UA treatment significantly relieved the injury of Nthy-ori 3-1 cells via inhibiting the ceRNA mechanism of MALAT1/miR-206/PTGS1 and inflammatory pathways, insinuating that UA may be helpful for the treatment of AIT.
Annotations
External Annotation for MALAT1 |
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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. |
