The Affiliated Nanhua Hospital, Department of Hematology, Hengyang Medical School, University of South China, Hengyang, China.
The Affiliated Nanhua Hospital, Department of Pain Treatment, Hengyang Medical School, University of South China, Hengyang, China.
Thorac Cancer. 2022 May;13(9):1406-1418. doi: 10.1111/1759-7714.14408. Epub 2022 Apr 7.
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.
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.
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.
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.
非小细胞肺癌（NSCLC）是全球导致癌症相关死亡的主要原因之一。本研究旨在阐明环状 RNA_0020123（circ_0020123）在 NSCLC 进展中的作用及其相关机制。
通过逆转录定量聚合酶链反应（RT-qPCR）和 Western blot 分析测定 RNA 和蛋白质表达。分析 circ_0020123/微小 RNA-512-3p（miR-512-3p）/冠状蛋白 1C（CORO1C）轴在 NSCLC 细胞中的作用，评估细胞增殖、迁移、侵袭、血管生成、凋亡和自噬。分析裸鼠的肿瘤发生，以确定 circ_0020123 在体内的作用。通过双荧光素酶报告和 RNA 免疫沉淀（RIP）测定证实了分子间靶关系。
circ_0020123 在 NSCLC 组织和细胞系中表达异常上调。circ_0020123 干扰显著抑制 NSCLC 细胞的增殖、迁移、侵袭、血管生成和自噬，并诱导细胞凋亡。circ_0020123 敲低抑制体内异种移植肿瘤生长。circ_0020123 作为 miR-512-3p 的分子海绵。circ_0020123 沉默诱导的 NSCLC 细胞的作用被 miR-512-3p 的敲低所逆转。miR-512-3p 与 CORO1C 的 3'非翻译区（3'UTR）相互作用。CORO1C 的过表达很大程度上逆转了 miR-512-3p 积累诱导的 NSCLC 细胞的影响。circ_0020123 通过在 NSCLC 细胞中结合 miR-512-3p 来正向调节 CORO1C 的表达。
circ_0020123 通过结合 miR-512-3p 来诱导 CORO1C 的表达，从而加剧 NSCLC 的进展，为 NSCLC 的治疗提供了新的潜在靶点。
