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Galectin-3 expression alters adhesion, motility and invasion in a lung cell line (DLKP), in vitro.
Authors: O'Driscoll L, Linehan R, Liang YH, Joyce H, Oglesby I, Clynes M.
Source: Anticancer Res 2002 Nov-Dec;22(6A):3117-25
National Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland. Lorraine.ODriscoll@dcu.ie
BACKGROUND: Galectin-3, a beta-galactosidase-binding protein, is involved in regulating many physiological and pathological cellular processes. The significance of galectin-3 in human lung and nasal carcinoma cells has not yet been elucidated. MATERIALS AND METHODS: Using RT-PCR and Western blotting techniques, the constitutive level of galectin-3 in the human non-small cell lung carcinoma cell line, DLKP, was investigated. Following galectin-3 cDNA transfection into these cells, growth, toxicity, adhesion, motility and invasion assays were used to investigate the relevance of galectin-3 over-expression. RESULTS: Galectin-3 over-expression did not induce a multi-drug resistance phenotype or significantly affect cell growth rate, but it did result in enhanced (i) adhesion to extracellular matrix components; (ii) cell motility; and (iii) in vitro invasiveness. Furthermore, studies of RPMI-2650 variants suggest that galectin-3 expression correlates with nasal carcinoma cell invasiveness. CONCLUSION: Our results suggest that galectin-3 expression levels in both lung and nasal tumour cells may play a role in cell motility, invasion, and metastasis.