Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieDiabetic Nephropathy
CeRNA1CDKN2B-AS1[LncRNA]
miRNAmiR-15b-5p[miRNA]
CeRNA2WNT2B[mRNA]
Tissue/Cell linehuman mesangial cells
SpecieHomo sapiens (human)
CitationDiabetol Metab Syndr. 2020 Dec 9;12(1):109. doi: 10.1186/s13098-020-00618-z.
Reference title
Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis.
Experimental verification
Dual-luciferase reporter assay;ELISA;Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;
Functional description
BACKGROUND: Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be related to diabetic nephropathy (DN) progression. However, the regulatory mechanisms of CDKN2B-AS1 in DN are unclear. METHODS: High glucose (HG) was used to induce human mesangial cells (HMCs) for establishing the DN model. Expression levels of CDKN2B-AS1, microRNA (miR)-15b-5p, wingless-Type family member 2B (WNT2B) mRNA in serum and HMCs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). The viability and cell cycle progression of HMCs were determined with Cell Counting Kit-8 (CCK-8) or flow cytometry assays. The levels of several proteins and inflammatory factors in HMCs were analyzed by western blotting or enzyme-linked immunosorbent assay (ELISA). The relationship between CDKN2B-AS1 or WNT2B and miR-15b-5p was verified with dual-luciferase reporter assay. RESULTS: CDKN2B-AS1 and WNT2B were upregulated while miR-15b-5p was downregulated in serum of DN patients and HG-treated HMCs. CDKN2B-AS1 inhibition reduced HG-induced viability, cell cycle progression, ECM accumulation, and inflammation response in HMCs. CDKN2B-AS1 regulated WNT2B expression via competitively binding to miR-15b-5p. MiR-15b-5p inhibitor reversed CDKN2B-AS1 knockdown-mediated influence on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs. The repressive effect of miR-15b-5p mimic on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs was abolished by WNT2B overexpression. CONCLUSION: CDKN2B-AS1 regulated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation response via regulating the miR-15b-5p/WNT2B axis, provided a new mechanism for understanding the development of DN.
Annotations
External Annotation for CDKN2B-AS1 |
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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. |
