Circular RNA PRKCI silencing represses esophageal cancer progression and elevates cell radiosensitivity through regulating the miR-186-5p/PARP9 axis

Abstract

AimsCircular RNA PRKCI (circPRKCI) and poly ADP-ribose polymerase 9 (PARP9) are related to the development of cancers. In this study, we aimed to explore the regulatory mechanisms between circPRKCI and PARP9 in EC progression and radioresistance. Materials and methodsThe levels of circPRKCI, PARP9 mRNA, and miR-186-5p were assessed by quantitative real time polymerase chain reaction (qRT-PCR). Western blot analysis was employed to examine the levels of several proteins. The viability, colony formation, cell cycle progression, and apoptosis of EC cells were determined with CCK-8, colony formation, or flow cytometry assays. The relationship between circPRKCI or PARP9 and miR-186-5p was verified with the dual-luciferase reporter and RIP assays. Key findingsWe observed that circPRKCI and PARP9 were upregulated while miR-186-5p was downregulated in EC tissues and cells. Furthermore, circPRKCI knockdown decreased tumor growth in vivo and constrained cell viability, colony formation, cell cycle progression, elevated cell radiosensitivity in EC cells in vitro. Importantly, circPRKCI modulated PARP9 expression through sponging miR-186-5p. Besides, PARP9 overexpression overturned circPRKCI silencing-mediated effects on the viability, colony formation, cell cycle progression, and radiosensitivity of EC cells. SignificanceCircPRKCI regulated cell malignancy and radioresistance through modulating the miR-186-5p /PARP9 axis in EC, which provided a might target for EC treatment.