Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieNasopharyngeal Cancer
CeRNA1SNHG6[LncRNA]
miRNAmiR-26a-5p[miRNA]
CeRNA2ARPP19[mRNA]
Tissue/Cell lineNPC tissues and cell
SpecieHomo sapiens (human)
CitationBioorg Med Chem Lett. 2021 May 15;40:127955. doi: 10.1016/j.bmcl.2021.127955. Epub 2021 Mar 17.
Reference title
LncRNA SNHG6 accelerates nasopharyngeal carcinoma progression via modulating miR-26a-5p/ARPP19 axis.
Experimental verification
qPCR;RT-qPCR;RIP assay;RNA pull-down assay;RNA pull-down;
Functional description
OBJECTIVES: Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. DESIGN: Prospective feasibility study. SETTING: The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital. Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. RT-qPCR assay was used to examine the expression of SNHG6, miR-26a-5p, and ARPP19 in NPC. CCK-8 and transwell assays were employed to detect NPC cell viability, migration, and invasion. The interaction between miR-26a-5p and SNHG6 or ARPP19 was determined by the luciferase reporter, RIP and RNA pull-down assays. We observed that SNHG6 expression was enhanced in NPC tissues and cells. SNHG6 deletion attenuated NPC cell viability and metastasis. MiR-26a-5p was predicted and validated to interact with SNHG6, and miR-26a-5p expression was markedly elevated in NPC after SNHG6 silence. Moreover, miR-26a-5p inhibitor rescued the suppressive effect of SNHG6 depletion on NPC cell viability, migration and invasion. Besides, ARPP19 was a target of SNHG6 and positively regulated by SNHG6. ARPP19 overexpression neutralized the repressive effect of SNHG6 knockdown on NPC progression. Our results indicated that SNHG6 regulated NPC progression through modulating miR-26a-5/ARPP19 axis, which might provide new insights into NPC diagnosis and treatment.
Annotations
External Annotation for SNHG6 |
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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. |
