ArticleBioengineered2021
Circular RNA circPRKDC promotes tumorigenesis of gastric cancer via modulating insulin receptor substrate 2 (IRS2) and mediating microRNA-493-5p.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The role of circular RNAs in gastric Cancer: Focusing on autophagy, EMT, and their crosstalk.Biochemistry and biophysics reports · 2025Review
- Buffalo bbu-miR-493-5p Promotes Myoblast Proliferation and Differentiation.Animals : an open access journal from MDPI · 2024Article
- Exploration and bioinformatic prediction for profile of mRNA bound to circular RNA BTBD7_hsa_circ_0000563 in coronary artery disease.BMC cardiovascular disorders · 2024Article
- The Insulin Receptor Substrate 2 Mediates the Action of Insulin on HeLa Cell Migration via the PI3K/Akt Signaling Pathway.Current issues in molecular biology · 2023Article
- Cancer-associated fibroblasts promote tumor cell growth via miR-493-5p in intrahepatic cholangiocarcinoma.Cancer science · 2023Article
- Noncoding RNAs and hyperthermic intraperitoneal chemotherapy in advanced gastric cancer.Bioengineered · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
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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