Circ_0026134 promotes NSCLC progression by the miR-3619-5p/CHAF1B axis.

Abstract

BackgroundNon‐small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. Circular RNAs (circRNAs) have been implicated in the pathogenesis of NSCLC. In this study, we explored the molecular determinants underlying the oncogenic property of circ_0026134 in NSCLC.MethodsThe levels of circ_0026134, miR‐3619‐5p and chromatin assembly factor 1 subunit B axis (CHAF1B) were assessed by quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blot. Cell colony formation, migration, invasion and apoptosis were detected by colony formation, Transwell, and flow cytometry assays, respectively. Direct relationships among circ_0026134, miR‐3619‐5p and CHAF1B were verified by dual‐luciferase reporter assays.ResultsOur results showed that circ_0026134 was highly expressed in NSCLC tissues and cells. Reduced circ_0026134 expression or miR‐3619‐5p overexpression inhibited NSCLC cell colony formation, migration, invasion, glycolysis and promoted cell apoptosis in vitro. Moreover, circ_0026134 directly targeted miR‐3619‐5p, and circ_0026134 regulated CHAF1B expression through miR‐3619‐5p. CHAF1B was a downstream effector of circ_0026134 in affecting NSCLC cell functional behaviors in vitro. Additionally, circ_0026134 silencing weakened tumor growth in vivo.ConclusionsOur study identified a novel regulatory mechanism, the circ_0026134/miR‐3619‐5p/CHAF1B axis, for the oncogenic role of circ_0026134 in NSCLC, highlighting circ_00261345 inhibition as a potential therapeutic method against NSCLC.