We demonstrated Galectin-3-induced TLR4/NF-κB signaling activation could contribute to lung adenocarcinoma cell proliferation and migration through p65 nucleus translocation and NEAT1 expression upregulation; Galectin-3/TLR4/NF-κB/NEAT1 path might be another contributor to the hyperproliferation and migration of lung adenocarcinoma cells. This evidence concerns the gene TLR4 and lung adenocarcinoma.