Abstract: Objective To investigate the effect of galectin-1 on biological behaviors of lung adenocarcinoma cells and the underlying mechanism. Methods The expression levels of galectin-1 mRNA were detected in 8 pairs of lung adenocarcinoma tissues and adjacent normal tissues and in lung adenocarcinoma cell lines A549 and H1299 and normal bronchial epithelial cell line BEAS-2b using qRT-PCR. The effect of galectin-1 knockdown by RNA interference on the proliferation, invasion and migration abilities and apoptosis of lung adenocarcinoma cells were examined using CCK8 assay, Transwell assay, scratch assay and flow cytometry. Western blotting was performed to detect the expressions of apoptosis-related proteins BAX, BCL-2, and caspase-3 and the proteins involved in the AKT and ERK pathways. Results The mRNA expression of galectin-1 was significantly increased in lung cancer tissues and lung adenocarcinoma cell lines (P<0.05). In lung adenocarcinoma cells, galectin-1 knockdown significantly inhibited cell proliferation, migration and invasion and obviously increased cell apoptosis rate (P<0.05), causing also significant reduction of the phosphorylation level of ERK signaling pathway (P<0.05). Conclusion Galectin-1 knockdown inhibits proliferation, migration, and invasion and promotes apoptosis of lung adenocarcinoma cells, and this effect is mediated probably by inhibition of the phosphorylation levels of the ERK pathway.

Key words: lung adenocarcinoma; galectin-1; proliferation; invasion; migration; apoptosis; ERK signaling pathway