LINC00885 promotes development of lung adenocarcinoma through AKT/mTOR/P70 signaling LINC00885 may regulate migration, proliferation, and invasion of lung adenocarcinoma through the mTOR pathway

Abstract

Abstract Purpose Previous studies have demonstrated the role of long non-coding RNAs (lncRNAs) in lung adenocarcinoma (LUAD). Methods Results RNA sequencing analysis identified high LINC00885 expression levels in LUAD, especially in the middle and advanced stages. Our functional experiments showed that knocking down expression of LINC00885 using small interfering RNAs inhibited the growth, migration, invasion, and autophagy of LUAD cells, blocked cell cycle progression, and promoted apoptosis. LINC00885 knockdown also reduced protein expression levels of p21, MET, p-mTOR, and p-P70, suggesting that LINC00885 may regulate the growth and metastasis of LUAD through these signaling pathways. Further experiments revealed that an mTOR activator rescued inhibited cell growth, invasion, and migration following LINC00885 knockdown. Conclusion These findings demonstrate that LINC00885 may promote LUAD by regulating p21, MET, and mTOR/P70 signal transduction. They also suggest that LINC00885 may be a prognostic biomarker and therapeutic target in LUAD.