Circular RNA circPRKDC promotes tumorigenesis of gastric cancer via modulating insulin receptor substrate 2 (IRS2) and mediating microRNA-493-5p.
Bioengineered
; 12(1): 7631-7643, 2021 12.
Article
em En
| MEDLINE
| ID: mdl-34605348
ABSTRACT
CircPRKDC has been disclosed to participate in the tumorigenesis of serval tumors, but the regulatory mechanisms of circPRKDC in GC are still unknown. CircPRKDC, miR-493-5p, and insulin receptor substrate 2 (IRS2) levels were tested by RT-qPCR. The epithelial-mesenchymal transition (EMT)-related protein levels were evaluated via western blot. The cell viability, migration and invasion were evaluated through CCK-8 and Transwell assays. Luciferase reporter and RIP assays were employed to confirm the binding ability between miR-493-5p and circPRKDC or IRS2. CircPRKDC was upregulated in GC samples, and circPRKDC silencing restrained GC cell viability, metastasis, and EMT and suppressed GC tumor growth. Besides, miR-493-5p was a target of circPRKDC, and the repressive impact of circPRKDC knockdown on GC development was neutralized by miR-493-5p inhibition. Moreover, miR-493-5p targeted IRS2 and IRS2 addition rescued the effects of circPRKDC depletion on GC progression. Finally, circPRKDC knockdown could regulate IRS2 expression by targeting miR-493-5p. These results elaborated that circPRKDC accelerated GC development via sponging miR-493-5p and increasing IRS2, which might provide novel potential targets for GC treatment.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Gástricas
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MicroRNAs
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Proteínas Substratos do Receptor de Insulina
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RNA Circular
Limite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Bioengineered
Ano de publicação:
2021
Tipo de documento:
Article