Non‐small cell lung cancer (NSCLC) has been considered to be the most common category of lung cancer, comprising approximately 80% of lung cancers. Long non‐coding RNAs (lncRNAs) were diffusely documented to modulate carcinogenesis or progression of tumours. However, the role of DDX11‐AS1 was still unclear in NSCLC. Bioinformatics analysis and experimental assays including hematoxylin and eosin (H&E) staining, RT‐qPCR, colony formation, CCK‐8, flow cytometry, western blot and xenograft assays were applied to investigate the biological role and molecular mechanism of DDX11‐AS1 in NSCLC. The level of lncRNA DDX11‐AS1 was up‐regulated in NSCLC tumour tissues and cells. In function aspect, knockdown of DDX11‐AS1 caused an apparent inhibitive effect on cell proliferation in vitro and in vivo. DDX11‐AS1 inhibition promoted cell apoptosis in vitro. In mechanism, the protein level of phosphorylated AKT was reduced by DDX11‐AS1 inhibition but increased by DDX11‐AS1 overexpression. These results indicated that DDX11‐AS1 exacerbated NSCLC progression via activating PI3K/AKT signalling pathway. All in all, DDX11‐AS1 promotes NSCLC development via regulating PI3K/AKT signalling.

中文翻译：

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长链非编码 RNA DDX11-AS1 通过调节 PI3K/AKT 信号传导促进非小细胞肺癌的发展。

非小细胞肺癌 (NSCLC) 被认为是最常见的肺癌类别，约占肺癌的 80%。长链非编码 RNA (lncRNA) 被广泛记录在案，可调节肿瘤的发生或进展。然而，DDX11-AS1 在 NSCLC 中的作用仍不清楚。应用生物信息学分析和实验分析，包括苏木精和伊红 (H&E) 染色、RT-qPCR、集落形成、CCK-8、流式细胞术、蛋白质印迹和异种移植分析，以研究 DDX11-AS1 在 NSCLC 中的生物学作用和分子机制。lncRNA DDX11-AS1水平在NSCLC肿瘤组织和细胞中上调。在功能方面，DDX11-AS1的敲低在体外和体内对细胞增殖产生明显的抑制作用。DDX11-AS1抑制促进体外细胞凋亡。在机制上，磷酸化 AKT 的蛋白质水平因 DDX11-AS1 抑制而降低，但因 DDX11-AS1 过表达而增加。这些结果表明 DDX11-AS1 通过激活 PI3K/AKT 信号通路加剧了 NSCLC 的进展。总而言之，DDX11-AS1 通过调节 PI3K/AKT 信号传导促进 NSCLC 的发展。