Detail (Experimental CeRNA)

Home Detail(Experimental CeRNA)

Basic Information

Regular Relationship :


Phenotype/DiseaseSpecie

Ovarian Cancer

CeRNA1

MALAT1[LncRNA]

miRNA

miR-1271-5p[miRNA]

CeRNA2

E2F5[mRNA]


Tissue/Cell line

OC tissues and cells

Specie

Homo sapiens (human)

Citation

Cancer Manag Res. 2020 Oct 12;12:9999-10010. doi: 10.2147/CMAR.S261979. eCollection 2020.


Reference title
LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis.
Experimental verification
Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;

Functional description
BACKGROUND: Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) were reported to be related to the development of ovarian cancer (OC). In this study, the functional mechanisms of lncRNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) and microRNA-1271-5p (miR-1271-5p) were explored in OC. METHODS: The level of MALAT1, miR-1271-5p, or E2F transcription factor 5 (E2F5) was detected by qRT-PCR. MTT assay, flow cytometry analysis and transwell migration and invasion assays were performed to determine cell proliferation, apoptosis, migration and invasion, respectively. E2F5 protein expression was detected by Western blot. The interaction between miR-1271-5p and MALAT1 or E2F transcription factor 5 (E2F5) was confirmed by the dual-luciferase reporter assay. RESULTS: MALAT1 and E2F5 level were increased, while miR-1271-5p level was decreased in cisplatin (DDP)-resistant OC tissues and cells. MALAT1 knockdown or miR-1271-5p upregulation decreased IC(50) of cisplatin, and inhibited cell proliferation, migration, invasion, and facilitated cell apoptosis in DDP-resistant OC cells. Moreover, MALAT1 sponged miR-1271-5p to upregulate E2F5 expression. Besides, MALAT1 knockdown decreased DDP resistance, inhibited cell proliferation, migration, invasion, and promoted cell apoptosis by sponging miR-1271-5p to downregulate E2F5 expression in DDP-resistant OC cell. CONCLUSION: We demonstrated that MALAT1 mediated DDP-resistant OC development through miR-1271-5p/E2F5 axis, providing the theoretical basis for OC therapy.

Annotations

External Annotation for MALAT1
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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