As one of the three major malignant tumors, lung adenocarcinoma (LUAD), with its rapid progression and high mortality rate, has become the most dangerous factor endangering human health. This study aims to explore new potential molecular targets, explore the regulatory role of lncRNA APTR in LUAD, and provide a more theoretical basis for the selection of LUAD therapeutic targets. The expression of APTR in LUAD was detected by PCR experiments, and the relationship between APTR and patients' clinical conditions and prognosis was analyzed by chi-square test, multifactor Cox regression, and Kaplan-Meier. The interaction between APTR and miR-298 and the regulation of LUAD cellular activities by APTR/miR-298 were explored by the luciferase reporter gene system. APTR expression was found to be upregulated in LUAD tissues and cells, and the expression of APTR was revealed to be substantially linked with lymph node metastases and TNM stage. High expression of LUAD also predicted a poor prognosis for patients. Downregulation of APTR expression significantly inhibited the activities of LUAD cells. In addition, APTR targeted miR-298 and negatively regulated miR-298 expression. The inhibitory effect of APTR knockdown on LUAD cell activity was also reversed after transfection with miR-298 inhibitor. Increasing expression of APTR is associated with patients' poor prognosis, APTR targets miR-298 and promotes LUAD cellular activity through negative regulation of miR-298.