Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieGastric Cancer
CeRNA1ANRIL[LncRNA]
miRNAmiR-181a-5p[miRNA]
CeRNA2CCNG1[mRNA]
Tissue/Cell lineGastric Cancer Cells
SpecieHomo sapiens (human)
CitationOncol Lett. 2021 Aug;22(2):621. doi: 10.3892/ol.2021.12882. Epub 2021 Jun 28.
Reference title
Effects of lncRNA ANRIL-knockdown on the proliferation, apoptosis and cell cycle of gastric cancer cells.
Experimental verification
Western blot;Flow Cytometry assay;Luciferase reporter assay;
Functional description
Gastric cancer is one of the most common types of malignant tumor of the gastrointestinal tract worldwide. Cisplatin (DDP) is a commonly used chemotherapeutic drug in the clinic; however, the resistance of gastric cancer cells to DDP limits its efficacy. In the present study, drug-resistant gastric cancer cell lines were constructed using the stepwise continuous selection method, and the relative expression levels of long non-coding RNA (lncRNA) CDKN2B antisense RNA 1 (ANRIL) and microRNA (miR)-181a-5p were detected using reverse transcription-quantitative PCR. The knockdown of lncRNA ANRIL and miR-181a-5p expression was performed by transfection with shRNA-ANRIL and an miR-181a-5p inhibitor, respectively. Cellular proliferation and sensitivity to DDP were assessed using Cell Counting Kit-8 analysis. Cell apoptosis and cell cycle distribution were assessed using flow cytometry and western blotting. The binding relationships between ANRIL, miR-181a-5p and cyclin G1 (CCNG1) were verified using a dual luciferase reporter assay. The results revealed that the expression levels of miR-181a-5p were downregulated in all drug-resistant cell lines. ANRIL-knockdown inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest; however, following the knockdown of miR-181a-5p, the inhibition of cell cycle arrest was alleviated. Notably, miR-181a-5p, ANRIL and CCNG1 were found to have targeting relationships. In conclusion, the findings of the present study suggested that knocking down the expression of ANRIL inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest. Furthermore, its downstream target, miR-181a-5p, inhibited the proliferation of drug-resistant cells and enhanced their sensitivity to DDP.
Annotations
External Annotation for ANRIL |
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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. |
