Detail (Experimental CeRNA)

Home Detail(Experimental CeRNA)

Basic Information

Regular Relationship :


Phenotype/DiseaseSpecie

Renal Cancer

CeRNA1

FGD5-AS1[LncRNA]

miRNA

miR-5590-3p[miRNA]

CeRNA2

NA[mRNA]


Tissue/Cell line

renal cancer cells

Specie

Homo sapiens (human)

Citation

Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8756-8766. doi: 10.26355/eurrev_202009_22814.


Reference title
LncRNA FGD5-AS1/miR-5590-3p axis facilitates the proliferation and metastasis of renal cell carcinoma through ERK/AKT signalling.
Experimental verification
qPCR;RT-qPCR;Western blot;luciferase assay;RNA pull-down;

Functional description
OBJECTIVE: Amongst noncoding RNAs, competing endogenous RNAs (ceRNAs) are popular and interesting regulatory mechanisms involved in oncogenesis and tumour progression. LncRNA FGD5-AS1, also known as miR-5590-3p, is involved in the regulatory role of ceRNA in many cancers. However, the roles of lncRNA FGD5-AS1 or miR-5590-3p in renal cell carcinoma (RCC) remain unclear. We investigated how FGD5-AS1 and miR-5590-3p regulated clear cell proliferation and metastasis in RCC. PATIENTS AND METHODS: Real Time-quantitative PCR (RT-qPCR) was used to detect the expression of FGD5-AS1 in tumour issues and renal cancer cell lines. MTT, scratch test and transwell assay were performed to confirm the effect of FGD5-AS1 on the proliferation, migration or invasion of the above cell lines. RNA pull-down and Luciferase assays were used to detect the target site between FGD5-AS1 and miR-5590-3p. In addition, we examined the proteins related to ERK/AKT signalling related via Western blot analysis. Finally, we used the RT-qPCR method to detect the mRNA levels of E-cadherin and vimentin. RESULTS: LncRNA FGD5-AS1 was highly expressed in renal cancer tissues, especially in patients with metastasis. This effect facilitated the proliferation, migration, epithelial-mesenchymal transition and invasion of renal cancer cells. Silencing the expression of FGD5-AS1 with FGD5-AS1 siRNA significantly inhibited the malignancy of tumour cells. RNA pull-down and Luciferase assays demonstrated that FGD5-AS1 targeted miR-5590-3p to interact with miR-5590-3p negatively. Furthermore, miR-5590-3p inhibitors could eliminate the FGD5-AS1 siRNA-induced upregulation of E-cadherin and downregulation of vimentin. CONCLUSIONS: Mechanistically, lncRNA FGD5-AS1 can competitively interact with miR-5590-3p and regulate the downstream signalling of ErkAKT to enhance the malignancy of tumours. This lncRNA could become a potential target molecule for treating and diagnosing RCC.

Annotations

External Annotation for FGD5-AS1
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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