Objective: The carcinogenic effects of circular RNA circ-PRKCI have been recognized in a variety of malignancies. However, the exact biological function of circ-PRKCI in gastric cancer has not been fully elucidated. Therefore, the aim of this study was to explore the expression of circ-PRKCI in gastric cancer (GC) and to investigate its potential regulation mechanism in the pathogenesis and progression of GC.
Patients and methods: The expression of circ-PRKCI in 50 GC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Statistical methods were used to analyze the relation between circ-PRKCI expression and overall survival rate of patients. The effect of circ-PRKCI on GC cell proliferation was examined by cell counting kit-8 (CCK-8) and cell colony formation assays. Meanwhile, the effect of circ-PRKCI on the invasion ability of GC cells was determined by transwell invasion assay. Flow cytometry was used to detect the apoptosis of GC cells. Bioinformatics was used to search for miRNAs that might have direct effects with circ-PRKCI. In addition, the binding of circ-PRKCI to microRNA-545 was validated using Dual-Luciferase reporter gene assay.
Results: Circ-PRKCI was significantly highly expressed in GC tissues, as well as cell lines. High expression of circ-PRKCI was positively associated with a poor prognosis of GC patients. Overexpression of circ-PRKCI significantly promoted the proliferation and invasion of GC cells, whereas reduced the proportion of apoptotic GC cells. Subsequent Dual-Luciferase reporter gene assay revealed that circ-PRKCI could bind to microRNA-545 and inhibit its expression in GC cells. These results indicated that circ-PRKCI might promote the development of GC by adsorbing microRNA-545 in a sponge manner.
Conclusions: Circ-PRKCI can be used as a potential prognostic indicator of GC, providing a new perspective for the potential bio-molecular mechanism in GC.