SLITRK6 promotes the progression of lung adenocarcinoma by regulating PI3K/AKT/mTOR signaling and Warburg effect.

Abstract

To investigate the role of SLITRK6 in lung adenocarcinoma (LUAD) and the underlying mechanism in it, clinical tissues and tissue microarray of LUAD were used to detect the expression of SLITRK6. In vitro cell viability assay and colony formation assay in LUAD cells were conducted to investigate SLITRK6 related biological functions. In vivo subcutaneous model was used to determine the role of SLITRK6 in LUAD growth. It was found that the expression of SLITRK6 was significantly upregulated in LUAD tissues compared with that in para-cancerous tissues. Knockdown of SLITRK6 suppressed the proliferation and colony formation of LUAD cells in vitro. Meanwhile, the growth of LUAD cells was also inhibited by SLITRK6 knockdown in vivo. Furthermore, we found that SLITRK6 knockdown could suppress the glycolysis of LUAD cells by regulating the phosphorylation of AKT and mTOR. All results suggest that SLITRK6 promotes LUAD cell proliferation and colony formation by regulating PI3K/AKT/mTOR signaling and Warburg effect. SLITRK6 may serve as a potential therapeutic target for LUAD in future.