Detail (Experimental CeRNA)

Home Detail(Experimental CeRNA)

Basic Information

Regular Relationship :


Phenotype/DiseaseSpecie

Rectal Cancer

CeRNA1

EGOT[LncRNA]

miRNA

miR-211-5p[miRNA]

CeRNA2

ErbB4[mRNA]


Tissue/Cell line

rectal cancer tissues and cells

Specie

Homo sapiens (human)

Citation

Onco Targets Ther. 2021 Apr 28;14:2867-2878. doi: 10.2147/OTT.S256989. eCollection 2021.


Reference title
LncRNA EGOT/miR-211-5p Affected Radiosensitivity of Rectal Cancer by Competitively Regulating ErbB4.
Experimental verification
Dual-luciferase reporter assay;qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;

Functional description
BACKGROUND/AIMS: Long non-coding ribonucleic acids (lncRNAs) are involved in the progression of cancers and affect the response to radiation therapy. This study was to investigate the mechanism of lncRNA EGOT in the radiosensitivity of rectal cancer. METHODS: The mRNA expression of EGOT, miR-211-5p and ErbB4 in rectal cancer tissues and cells was detected by qRT-PCR. The protein expression of ErbB4 was detected by Western blot. Dual-luciferase reporter assay and ribonucleic acid immunoprecipitation (RIP) were used to confirm the interaction between EGOT and miR-211-5p or miR-211-5p and ErbB4. Transfection technology was used to down-regulate and up-regulate the expression of EGOT and miR-211-5p in rectal cancer cells, respectively. MTT, colony formation and flow cytometry were used to detect the effect of EGOT and miR-211-5p on proliferation, invasion, migration and apoptosis of rectal cancer cells. RESULTS: The expression of EGOT was up-regulated in rectal cancer tissues and cells, and the expression of EGOT was related to the late stage of pathology. EGOT knockdown inhibited the proliferation and colony formation of rectal cancer cells and induced the apoptosis of rectal cancer cells. Moreover, EGOT knockdown was significantly enhanced the effects of radiotherapy on rectal cancer in vivo and in vitro. Furthermore, EGOT was found to serve as a sponge of miR-211-5p, and ErbB4 was a downstream target of miR-211-5p. EGOT enhanced the expression of ErbB4 by regulating miR-211-5p. MiR-211-5p inhibitor restored the effect of EGOT knockdown on the radiosensitivity of rectal cancer. CONCLUSION: Down-regulation of EGOT could inhibit the growth of rectal cancer cells by regulating the miR-211-5p/ErbB4 axis and improve the radiosensitivity of rectal cancer cells. EGOT may be a new therapeutic target for rectal cancer.

Annotations

External Annotation for EGOT
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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