Role and regulation mechanism of Gal-3 in non-small cell lung cancer and its potential clinical therapeutic significance

Galectin-3 (Gal-3), the only chimeric lectin of the galectin family, affects numerous biological processes and seems to be involved in different physiological and pathophysiological conditions, such as tumor development, invasion and metastasis as well as immune reactions. There is growing evidence to show that Gal-3 participates in the tumorigenesis, invasion and metastasis as well as tumor immunity in non-small cell lung cancer (NSCLC). A better understanding of the molecular mechanisms of Gal-3 involved in NSCLC development is avidly needed as the basis to identify novel therapeutic targets and develop new strategies for the treatment of NSCLC. In this review, we summarized the distribution and expression of Gal-3 in NSCLC which is highly expressed in NSCLC than in normal lung tissues, and the molecular regulation mechanism of Gal-3 in the development of NSCLC, including upregulation of Wnt/β-catenin pathway and EGFR expression, involvement in Notch signaling pathway, etc. Moreover, Gal-3 promoted the invasion and metastasis of NSCLC through induction of MMPs secretion, cooperation with integrins, and interaction with mucin 1 to promote cancer-endothelial adhesion. Furthermore, Gal-3 binded to Poly-N-acetyl-lactosamine on N-glycans to promote NSCLC metastasis as well as contributing to tumor microenvironment immunosuppression, which might provide potential therapeutic implications for the clinical treatment of NSCLC. •Gal-3 is highly expressed in NSCLC than in normal lung tissues.•Gal-3 promotes the development of NSCLC by regulating β-catenin and EGFR.•Gal-3 promotes the migration of NSCLC by regulating MMPs, integrin and MUC1.•Gal-3 contributes to tumor microenvironment immunosuppression in NSCLC.•Gal-3 may be a therapeutic target and an indicator of the poor prognosis in NSCLC.