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This study investigated the prognostic value and molecular mechanisms of miR-517c-3p in lung cancer. miR-517c-3p in 112 lung cancer tissues was detected using qRT-PCR. Kaplan-Meier survival analysis and Cox regression were used to assess its prognostic significance. Functional experiments, including cell proliferation, migration, and invasion, were conducted in lung cancer cell lines (H1229, A549) after miR-517c-3p overexpression. Target gene prediction and validation were performed using bioinformatics tools and dual-luciferase reporter assays. The regulatory effects of miR-517c-3p on ARNTL2 were further explored through gene overexpression and rescue experiments. miR-517c-3p was significantly downregulated in lung cancer tissues (p < 0.001) and correlated with advanced TNM stage, lymph node metastasis, and larger tumor size. Patients with low miR-517c-3p expression exhibited poorer overall survival (p < 0.001), and Cox regression identified miR-517c-3p as an independent prognostic factor (HR = 0.110, 95% CI = 0.047-0.256). Functional assays demonstrated that miR-517c-3p overexpression inhibited lung cancer cell proliferation, migration, and invasion. Dual-luciferase reporter assays confirmed ARNTL2 as a direct target of miR-517c-3p, and ARNTL2 restoration reversed the suppressive effects of miR-517c-3p on tumor progression. miR-517c-3p is significantly downregulated in lung cancer and associated with poor patient prognosis. Furthermore, miR-517c-3p suppresses tumor progression by directly targeting ARNTL2.