BACKGROUND: Lung adenocarcinoma (LUAD) is a major contributor to global mortality. Grounded onto bioinformatics insights, this study probes the functions of dynein light chain LC8-type 1 (DYNLL1) in LUAD progression. METHODS: DYNLL1 levels in LUAD and normal cells were determined using qPCR and western blotting analyses. Lentiviral plasmids-mediated DYNLL1 silencing was induced in LUAD cells, followed by functional assays to investigate DYNLL1's impacts on proliferation, mobility, apoptosis, and cell cycle distribution. KY19382, a Wnt/β-catenin agonist, was employed to analyze the involvement of the Wnt/β-catenin pathway in DYNLL1's effects. Upstream regulator of DYNLL1 was queried using bioinformatics. Mouse LUAD cells LA795 were implanted into BALB/c nude mice to establish animal tumor models. RESULTS: DYNLL1 exhibited heightened expression in LUAD cells. Its artificial silencing reduced proliferation and dissemination of cancer cells, promoted cell apoptosis, and induced G0/G1 cell cycle arrest. DYNLL1 silencing reduced β-catenin levels in cancer cells, and KY19382 treatment diminished the effects induced by DYNLL1 silencing. TEA domain transcription factor 4 (TEAD4), upregulated in LUAD cells, binds to the DUNLL1 promoter for transcriptional activation. TEAD4 silencing in LUAD cells reduced DYNLL1 transcription and β-catenin levels, thus suppressing proliferation while promoting apoptosis, senescence, and cell cycle arrest. In vivo, TEAD4 silencing weakened tumorigenesis of LA795 cells. Nevertheless, these phenomena were counteracted by the artificial DYNLL1 restoration in LUAD cells. CONCLUSION: This investigation demonstrates a TEAD4-DYNLL1 axis that accelerates cell cycle progression and augments malignant properties of LUAD cells via the Wnt/β-catenin pathway.