Objective: We aimed to investigate the expression and specific molecular mechanism of circ-PRKCI in lung cancer (LCa).
Patients and methods: The relationship between the expression level of circ-PRKCI and the prognosis of patients was analyzed. The impacts of circ-PRKCI on the invasiveness of LCa cells were examined by Cell Counting Kit-8 (CCK-8) experiments, clone formation experiments, and transwell invasion experiments. Subcellular localization of circ-PRKCI was determined through nuclear separation experiments. Downstream target genes that can bind to circ-PRKCI was predicted through bioinformatics analysis, and was then verified by Dual-Luciferase experiments, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) experiments, and Western blot experiments.
Results: Circ-PRKCI level was remarkably elevated in LCa tumor tissues and cell lines. At the same time, highly expressed circ-PRKCI was correlated with the poor prognosis of LCa patients. In vitro cell experiments revealed that inhibition of circ-PRKCI in LCa cell lines remarkably inhibited cell invasiveness and proliferation. In addition, circ-PRKCI can compete with MECP2 to bind microRNA-1324 and thus affect the progression of LCa.
Conclusions: Our study shows for the first time that circ-PRKCI modulates the progression of LCa through microRNA-150-5p/MECP2 axis.