In this study, we verified that interfering with PSME3 resulted in decreased proliferative capacity of LUAD cells by CCK8, Transwell and clonal origin assays, and verified that PSME3 may affect apoptosis of lung adenocarcinoma cells through the PI3K/AKT/Bcl-2 signaling pathway by Western Blot, and found that PSME3 was associated with the bioinformatic immune checkpoints were significantly positively correlated, suggesting that PSME3 may be a novel target in the immunotherapy of lung adenocarcinoma. Here, PSME3 is linked to lung adenocarcinoma.