Objective <p>To investigate the impact of LINC00886 on the prognosis of patients with non-small cell lung cancer (NSCLC) and its regulatory effects on cancer cells.</p> Methods <p>A total of 184 NSCLC patients were enrolled. Postoperative tissues were preserved in liquid nitrogen. Kaplan - Meier (KM) survival curves were used to assess 5-year overall survival. Multivariate cox regression analysis was performed to identify independent prognostic factors for NSCLC. RT-qPCR detected gene expression levels. CCK-8 and Transwell assays evaluated cell proliferation, migration, and invasion. Dual-luciferase reporter assays validated the interaction between LINC00886 and miR-141-5p.</p> Results <p>Our study revealed that LINC00886 was markedly downregulated in both NSCLC tissues and cell lines. This reduced expression was significantly associated with larger tumor diameters and advanced TNM stages. Multivariate analysis identified LINC00886 as an independent protective factor for NSCLC patients, with its downregulation portending a lethal outcome. In vitro, ectopic expression of LINC00886 significantly attenuated the proliferation, migration, and invasion of NSCLC cells. We further identified miR-141-5p, which was upregulated in NSCLC, as a direct target gene of LINC00886. Critically, rescue experiments demonstrated that miR-141-5p mimics could abrogate the inhibition of LINC00886 overexpression on NSCLC cell function.</p> Conclusion <p>LINC00886 inhibits NSCLC cell proliferation, migration, and invasion through miR-141-5p, thereby suppressing NSCLC.</p>