Circ_0020123 plays an oncogenic role in non‐small cell lung cancer depending on the regulation of miR‐512‐3p/CORO1C

Abstract

Abstract Background Non‐small cell lung cancer (NSCLC) is one of the leading causes responsible for cancer‐associated death globally. The aim of this study was to illustrate the function of circular RNA_0020123 (circ_0020123) in NSCLC progression and its associated mechanism. Methods RNA and protein expression was determined by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) and western blot assay. Cell proliferation, migration, invasion, angiogenesis, apoptosis and autophagy were analyzed to assess the role of circ_0020123/microRNA‐512‐3p (miR‐512‐3p)/coronin 1C (CORO1C) axis in NSCLC cells. Tumorigenesis in nude mice was analyzed to determine the in vivo role of circ_0020123. The intermolecular target relation was confirmed by dual‐luciferase reporter and RNA immunoprecipitation (RIP) assays. Results Circ_0020123 expression was aberrantly upregulated in NSCLC tissues and cell lines. Circ_0020123 interference markedly restrained cell proliferation, migration, invasion, angiogenesis and autophagy and induced cell apoptosis of NSCLC cells. Circ_0020123 knockdown suppressed xenograft tumor growth in vivo. Circ_0020123 acted as a molecular sponge for miR‐512‐3p. Circ_0020123 silencing‐induced effects in NSCLC cells were largely reversed by the knockdown of miR‐512‐3p. miR‐512‐3p interacted with the 3′ untranslated region (3′UTR) of CORO1C. CORO1C overexpression largely reversed miR‐512‐3p accumulation‐induced influences in NSCLC cells. Circ_0020123 positively regulated CORO1C expression by sponging miR‐512‐3p in NSCLC cells. Conclusion Circ_0020123 aggravated NSCLC progression by binding to miR‐512‐3p to induce CORO1C expression, which provided new potential targets for the treatment of NSCLC.

Keywords

• angiogenesis
• circ_0020123
• CORO1C
• miR‐512‐3p
• non‐small cell lung cancer