LGALS3 and neoplasm: Consistent with above results, Galectin-3 overexpression significantly promoted, whereas CLI-095 remarkably suppressed the cell proliferation and migration of lung cancer cell lines; the above effects of Galectin-3 were partially eliminated by CLI-095 (Fig. 6c-e), indicating that Galectin-3 activates TLR4 signaling, followed by downstream NF-κB activation and NEAT1 expression upregulation, finally resulting in excessive proliferation and migration of tumor cells.