Expression of an endogenous galactose‐binding lectin correlates with neoplastic progression in the colon

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Abstract
Galectin-3 is an endogenous galactose-binding protein that is expressed in a wide range of normal and neoplastic tissues and is thought to be involved in cellular adhesion and growth regulation. Conflicting data have been reported regarding the expression of galectin-3 during carcinogenesis in the colon. The authors studied the expression of galectin-3 in 153 tissue specimens, including 29 adenomas containing early cancer, 66 colon carcinomas of known Dukes' stage with available long term patient survival data, and 23 additional primary carcinomas with 35 associated metastases. An immunohistochemical scoring system was used that considers tumor heterogeneity and yields an integrated numeric score subject to statistical analysis. Genetically related colon cancer cells with different metastatic capabilities also were compared by Western blot analysis. Galectin-3 expression was significantly higher in high grade dysplasia and early invasive cancers compared with the adenomatous tissue from which they evolved (mean staining score, 2.33 vs. 1.15; P = 0.001). Galectin-3 expression in invasive cancers varied according to Dukes' stage, indicating a linear relationship with advancing stage (P = 0.008). Enhanced expression correlated with decreased long term patient survival (P = 0.021). Metastases expressed a higher level of galectin-3 compared with the primary cancers from which they evolved (P < 0.005) as did cultured cells of high metastatic capability compared with their counterparts with low metastatic potential. Galectin-3 expression in colonic mucosa is related to neoplastic transformation and metastatic progression.