CircSEC24A induces KLF8 expression to promote the malignant progression of non‐small cell lung cancer by regulating miR‐1253

Abstract

ObjectivesThis study aimed to analyze the role of circSEC24A in non‐small cell lung cancer (NSCLC) and its underlying mechanism.MethodsRNA levels of circSEC24A, microRNA‐1253 (miR‐1253), and KLF transcription factor 8 (KLF8) were detected by quantitative real‐time polymerase chain reaction. Protein expression was analyzed by western blot or immunohistochemistry assay. Cell proliferation and apoptosis were investigated by colony formation assay, 5‐ethynyl‐2′‐deoxyuridine assay, and flow cytometry analysis. Glycolysis was evaluated by commercial kits. Dual‐luciferase reporter assay and RNA immunoprecipitation assay were conducted to identify the associations among circSEC24A, miR‐1253, and KLF8. Xenograft mouse model assay was used to evaluate the effect of circSEC24A on tumor tumorigenesis.ResultsCircSEC24A and KLF8 were upregulated, while miR‐1253 was downregulated in NSCLC. CircSEC24A knockdown inhibited proliferation and glycolysis but induced the apoptosis of NSCLC cells. CircSEC24A acted as a miR‐1253 sponge and regulated NSCLC cell malignancy by targeting miR‐1253. KLF8 was identified as a target of miR‐1253, and its overexpression attenuated miR‐1253‐induced effects in NSCLC cells. Besides, circSEC24A upregulated KLF8 by sponging miR‐1253. Further, circSEC24A knockdown suppressed NSCLC cell tumorigenesis in vivo.ConclusionsCircSEC24A silencing inhibited NSCLC cell malignancy through the miR‐1253/KLF8 pathway, providing a potential therapeutic target for NSCLC.