Abstract
Mounting evidence has demonstrated the important role of long non-coding RNAs (lncRNAs) in the development and progression of lung cancer. In this study, we combined the methods of bioinformatics analysis and experimental validation, and aim to investigate the clinical significance and underlying mechanism of the novel lncRNA AC079630.4 in lung cancer. Finally, we found that AC079630.4 was significantly down-regulated in lung cancer tissues, including in its subtypes. Samples with low AC079630.4 expression had a more advanced pathological stage and a worse prognosis than those with high expression. In functional prediction, the KEGG pathway of apoptosis and the TRAIL signaling pathway were enriched in the samples with high AC079630.4 expression. In experimental validation, AC079630.4 over-expression could significantly inhibit the proliferation and clonality, and up-regulated the receptors of TRAIL (TRAIL-R1 and TRAIL-R2) in lung cancer cells. In conclusion, we adopted the methods of bioinformatics analysis and experimental validation, and identified a novel lncRNA of AC079630.4 as a tumor suppressor in lung cancer.