Circ_0087862 promotes tumorigenesis and glycolysis in colorectal cancer by sponging miR-296-3p to regulate PGK1 expression

Abstract

BackgroundCircular RNAs (circRNAs) exert crucial roles in tumor progression of multiple cancers, including colorectal cancer (CRC). However, the functions of most circRNAs are not been fully elucidated. In this study, the role and mechanism of circ_0087862 in CRC were investigated. MethodsThe expression of circ_0087862, microRNA-296-3p (miR-296-3p) and phosphoglycerate kinase 1 (PGK1) was detected by quantitative real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2′-deoxyuridine (EdU) assay were used to assess cell proliferation. Flow cytometry was employed to analyze cell apoptosis. Transwell assay was employed to evaluate cell invasion. Western blot assay was employed to detect the level of related protein markers and PGK1. The glucose consumption, lactate production were tested by corresponding kits. The relationship between miR-296-3p and circ_0087862 or PGK1 was verified by dual-luciferase reporter assay or RNA immunoprecipitation (RIP) assay. The in vivo function of circ_0087862 was examined by xenograft mice model. ResultsThe expression levels of circ_0087862 and PGK1 were up-regulated in CRC tissues and cells, while miR-296-3p was down-regulated. Circ_0087862 silencing suppressed cell proliferation, invasion and glycolysis and promoted cell apoptosis in CRC cells. Circ_0087862 targeted miR-296-3p in CRC cells. MiR-296-3p inhibition reversed circ_0087862 silencing-mediated inhibition effect on cell proliferation, invasion and glycolysis, as well as the promotion effect on cell apoptosis. PGK1 was a target of miR-296-3p, and the overexpression of PGK1 attenuated miR-296-3p-mediated tumor suppression effect on CRC progression. Moreover, knockdown of circ_0087862 inhibited tumorigenesis in vivo. ConclusionCirc_0087862 promoted CRC progression via miR-296-3p/PGK1 axis and might act as a potential target for CRC therapy.