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.

为了探讨SLITRK6在肺腺癌（LUAD）中的作用及其潜在机制，采用临床组织和LUAD组织芯片检测SLITRK6的表达。通过LUAD细胞的体外细胞活力测定和集落形成测定来研究SLITRK6相关的生物学功能。使用体内皮下模型来确定 SLITRK6 在 LUAD 生长中的作用。结果发现，与癌旁组织相比，LUAD组织中SLITRK6的表达显着上调。SLITRK6 的敲除抑制了 LUAD 细胞的体外增殖和集落形成。同时，体内SLITRK6敲低也抑制了LUAD细胞的生长。此外，我们发现SLITRK6敲低可以通过调节AKT和mTOR的磷酸化来抑制LUAD细胞的糖酵解。所有结果表明SLITRK6通过调节PI3K/AKT/mTOR信号传导和Warburg效应促进LUAD细胞增殖和集落形成。SLITRK6可能成为未来LUAD的潜在治疗靶点。