Detail (Experimental CeRNA)

Home Detail(Experimental CeRNA)

Basic Information

Regular Relationship :


Phenotype/DiseaseSpecie

Non-Small Cell Lung Cancer

CeRNA1

hsa_circ_0058357[Circular RNA]

miRNA

miR-24-3p[miRNA]

CeRNA2

AVL9[mRNA]


Tissue/Cell line

NSCLC tissues and NSCLC cells

Specie

Homo sapiens (human)

Citation

Mol Med Rep. 2021 Jun;23(6):470. doi: 10.3892/mmr.2021.12109. Epub 2021 Apr 21.


Reference title
hsa_circ_0058357 acts as a ceRNA to promote non-small cell lung cancer progression via the hsa-miR-24-3p/AVL9 axis.
Experimental verification
Flow cytometry assay;Flow Cytometry assay;Immunoblotting;luciferase assay;

Functional description
Abnormal circular RNAs (circRNAs) are associated with biological processes in cancer; however, the function of circRNAs remains largely unknown in non-small cell lung cancer (NSCLC). The present study aimed to investigate the role of hsa_circ_0058357 on the progression of NSCLC. Cell proliferation, migration and apoptosis were determined using Cell Counting Kit-8, Transwell and flow cytometry assays, respectively. Gene [circRNA and microRNA (miR)] and protein expression levels were determined via reverse transcription-quantitative PCR and immunoblotting. A luciferase assay was employed to detect the binding of miR-24-3p with AVL9 cell migration associated (AVL9), while a cancer xenograft model was established to evaluate cancer growth in vivo. The results demonstrated that hsa_circ_0058357 was highly expressed in human NSCLC tissues and NSCLC cells compared with para-cancerous tissues and human bronchial epithelial (HBE) cells, respectively. Knockdown of hsa_circ_0058357 significantly suppressed cell viability, migration and tumor growth, while it promoted apoptosis in NSCLC cells. As a competing endogenous RNA, hsa_circ_0058357 knockdown contributed to the increase of miR-24-3p expression in NSCLC cells. Of note, overexpression of miR-24-3p markedly abolished the exogenous hsa_circ_0058357-induced excessive proliferation, migration and apoptosis resistance of NSCLC cells. Mechanistically, as a signaling molecule in late secretory pathway, AVL9 was also expressed at a high level in NSCLC tissues and cells, which could be directly suppressed by miR-24-3p. In the tumor tissues, along with growth inhibition, hsa_circ_0058357 knockdown also mediated the elevation of miR-24-3p and the reduction of AVL9. Thus, it was suggested that hsa_circ_0058357 may be a crucial regulation factor in NSCLC by sponging hsa-miR-24-3p, leading to a decrease in miR-24-3p expression, and subsequent increase in AVL9 expression. Therefore, hsa_circ_0058357 may serve as a potential target for diagnosis and gene therapy for NSCLC.

Annotations

External Annotation for hsa_circ_0058357
LncRNA-associated competing triplets and functions.
Comprehensive experimentally supported associations between lncRNA and human cancer.
Infer genomic variations that disturb lncRNA-associated ceRNA regulation..
Provide and annotate disease or phenotype-associated variants in human long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) or their regulatory elements.
Providing cellular-specific lncRNA-associated ceRNA networks predicted via high-throughput analysis of single-cell genomic data.
Information on all annotated and predicted human genes.
Gene nomenclature, gene families and associated resources (genomic, proteomic, phenotypic information).
Genome browser for vertebrate genomes.
An annotated collection of all publicly available DNA sequences.
A wiki-based platform for community curation of human long non-coding RNAs.
An integrated knowledge database dedicated to non-coding RNAs.
An integrated database of human annotated lncRNA transcripts.
Comprehensive annotations of eukaryotic long non-coding RNAs.
Comprehensive experimentally supported associations between lncRNA and human cancer.
A comprehensive, authoritative compendium of human genes and genetic phenotypes.
The catalogue of somatic mutations in cancer.

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