Galectin-3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is an epithelial carcinoma originating from the nasopharyngeal mucosal tissue and is highly prevalent in southeast Asia. Galectin-3 (gal-3) serves crucial roles in many cancers but its role in NPC remains to be elucidated. The aim of the present study was to investigate the role of gal-3 in NPC. Immunohistochemistry and ELISA were used to determine the expression level of gal-3 in patients with NPC or chronic rhinitis (CR). Gal-3 short hairpin (sh)RNA was established to knockdown gal-3 in 5–8F and 6–10B cells, allowing for the evaluation of the roles of gal-3 in proliferation, migration and apoptosis in NPC cell lines. Immunohistochemistry staining of IL-6 and IL-8 was applied to access the inflammatory state of tumor tissues, and the correlation between the inflammatory state and gal-3 was analyzed. The results demonstrated that gal-3 was upregulated in patients with NPC compared with patients with CR. Knockdown of gal-3 inhibited proliferation and migration in 5-8F and 6-10B cells, as well as promoted apoptosis in these cells. The expression levels of MMP-9 and IL-8 were also decreased in 5-8F and 6-10B cells after transfection with gal-3 shRNA. A positive correlation was identified between the expression level of gal-3 and the inflammatory state of NPC. The phosphorylation levels of ERK1/2 and Akt were downregulated after knockdown of gal-3 in 5-8F and 6-10B cells. In conclusion, the expression level of gal-3 was upregulated in patients with NPC and was positively correlated with the inflammatory state of NPC. The results suggested that gal-3 promoted the proliferation and migration of 5-8F and 6-10B cells, while inhibiting the apoptosis of these cells. Moreover, activation of ERK1/2 and Akt may be the underlying mechanism of the effects of gal-3 on NPC.