Abstract
Galectin-7 is a member of the β-galactoside-binding protein family, and is highly expressed in oral squamous cell carcinoma (OSCC). The aim of the present study was to investigate the effects of manipulating galectin-7 expression on the biological phenotype of human OSCC cells and the associated molecular mechanisms. Knockdown of endogenous galectin-7 via small interfering RNA (siRNA) was performed and cell proliferation, apoptosis, migration, and invasion were subsequently assessed. The data indicated that galectin-7 silencing had no impact on the proliferation or apoptosis of OSCC cells. However, compared with non-transfected cells, percentage wound closure was significantly lower in galectin-7-silenced cells following 24 h incubation, indicating decreased cell migration. Furthermore, Matrigel invasion assays demonstrated that galectin-7 knockdown significantly reduced the number of invaded cells, compared with the number in non-transfected cells. Western blot analysis indicated that galectin-7 overexpression resulted in a significant increase in the expression of the proteins matrix metalloproteinase (MMP)-2 and MMP-9. The invasive abilities of cells overexpressing galectin-7 significantly decreased following co-transfection with MMP-2- or MMP-9-specific siRNA. Increasing galectin-7 expression significantly enhanced the phosphorylation of extracellular signal-related kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) 1/2. Pharmacological inhibition of ERK or JNK activity significantly suppressed the invasiveness of galectin-7-overexpressing cells and abrogated the upregulation of MMP-2 and MMP-9. Taken together, the results of the current study provide novel evidence for the pro-invasive activity of galectin-7 in OSCC cells, which is associated with activation of ERK and JNK signaling and the induction of MMP-2 and MMP-9.