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.
Keywords: DDX11-AS1; NSCLC; PI3K/AKT signalling.
© 2020 John Wiley & Sons Australia, Ltd.