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

Abstract Previous studies have demonstrated a role for long non-coding RNAs in lung adenocarcinoma (LUAD). Here, we found high expression levels of LINC00885 in LUAD, especially in middle and advanced stage disease, by RNA-sequencing analysis. This suggests that LINC00885 may be a potential prognostic biomarker of LUAD. Our functional experiments showed that knocking down LINC00885 expression with small interfering RNAs inhibited the growth, migration, invasion, and autophagy of LUAD cells, blocked cell cycle progression, and promoted cell apoptosis. Additionally, LINC00885 knockdown reduced the 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. Additional experiments revealed that an mTOR activator rescued the inhibited cell growth, invasion, and migration following LINC00885 knockdown. Together, these findings demonstrate that LINC00885 may promote LUAD by regulating p21, MET, and mTOR/p70 signal transduction. This study suggests that LINC00885 may be a prognostic biomarker and therapeutic target in LUAD.