Background
Increasing evidence indicates that circular RNAs (circRNAs) act as vital regulators in various cancers. Nevertheless, the effect of circCSNK1G1 on gastric cancer (GC) is still unknown.
Conclusion
Our study revealed that circCSNK1G1 accelerated GC progression via the miR-758/ZNF217 axis, suggesting that circCSNK1G1 might be a potential biomarker for GC diagnosis and treatment.
Methods
The mRNA levels of circCSNK1G1, miR-758, and ZNF217 were measured by RT-qPCR. The protein levels of ZNF217 were evaluated by Western blotting. Cell migration, invasion, proliferation, and apoptosis were detected by Transwell, CCK-8, and flow cytometry assays. The association between miR-758 and circCSNK1G1/ZNF217 was confirmed by RIP and luciferase reporter assays. Xenograft assay was employed for in vivo experiment.
Results
In the current study, it was demonstrated that the expression levels of circCSNK1G1 and ZNF217 were upregulated in GC tissues and cells, while the level of miR-758 was declined. Furthermore, functional assays indicated that circCSNK1G1 depletion suppressed GC progression in vitro and in vivo. In addition, circCSNK1G1 directly interacted with miR-758, and the supplementation of miR-758 suppressed the development of GC, which was abolished following pcDNA3.1-circCSNK1G1 transfection. Then, we explored the downstream mechanism of miR-758 and found that miR-758 could target the 3'UTR of ZNF217 mRNA. The overexpression of miR-758 neutralized the ZNF217-mediated effects on facilitating the progression of GC. Finally, we revealed that circCSNK1G1 could upregulate ZNF217 expression by sponging miR-758 in GC cells.