Abstract
Focusing on the role of normal mucosa of esophagus specific 1 (NMES1) in LUAD, TCGA database was hereby first used to explore the expression and prognostic value of NMES1 in LUAD patients. qRT-PCR, Western blotting and immunohistochemistry were utilized to detect expression of NMES1. NMES1 expression was up-regulated in LUAD patients and LUAD cells. Subsequently, siRNA was utilized to transfect LUAD cells to knockdown NMES1. Proliferation, migration and invasion potential were evaluated by cell counting Kit-8, wound healing and transwell migration. Furthermore, experiments were also conducted to investigate the potential mechanisms. Finally, a transplanted tumor model was established to elucidate the functions of NMES1 on the tumorigenesis of LUAD cells. Knockdown of NMES1 notably inhibited proliferation, migration, cell cycle and tumor growth in xenografts. The findings demonstrated the efficiency of NMES1 in mediating the ROS level and Mitochondrial potential to promote PI3K/AKT signaling pathway.