ERO1L Promotes NSCLC Invasion via ROS‐Mediated EMT

This study investigates the effect of lentivirus-mediated ERO1L silencing on non-small cell lung cancer (NSCLC) cell invasion and migration and explores its underlying molecular mechanisms. RO1L expression was examined in NSCLC tissues. A549 cells with ERO1L silencing or overexpression were assessed for migration, invasion, proliferation, EMT markers, MMP expression, and ROS levels. The ROS scavenger N-acetylcysteine (NAC) was used to verify ROS involvement. ERO1L was significantly upregulated in NSCLC tissues. Silencing ERO1L reduced ROS production, inhibited cell migration, invasion, proliferation, and reversed EMT and MMP expression, whereas overexpression produced opposite effects. NAC treatment diminished ERO1L-induced ROS elevation and partially restored EMT markers and MMP levels, confirming a ROS-dependent mechanism. ERO1L promotes NSCLC cell invasion, migration, and proliferation through a ROS-dependent regulatory mechanism involving EMT markers and MMP expression. ERO1L may serve as a potential therapeutic target for NSCLC.