Upregulation of galectins-1 and -3 in human colon cancer and their role in regulating cell migration

✍ Scribed by Axel Hittelet; Hugues Legendre; Nathalie Nagy; Yves Bronckart; Jean-Claude Pector; Isabelle Salmon; Paul Yeaton; Hans-Joachim Gabius; Robert Kiss; Isabelle Camby

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: French
• Weight: 511 KB
• Volume: 103
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.10843

✦ Synopsis

Abstract

To probe the potential contribution of β‐galactoside‐contributing epitopes and receptor proteins (gal‐1 and gal‐3) to colon malignancy, we first examined the expression of galectins and binding sites in clinical specimens by lectin and immunohistochemistry. Sixty‐seven colonic surgical resections were studied, including 10 normal, 10 mild dysplasias, 10 severe dysplasias and 37 cancers. gal‐1 and gal‐3 were expressed in variable amounts in the epithelial cells and the connective tissue of normal colon. Their expression significantly increased with the degree of dysplasia, suggesting that gal‐1 and gal‐3 and their binding sites are related to malignant progression, while gal‐8 has been associated with suppressor activity. To study the functional aspects, the influence of these galectins on the migration of 4 human colorectal cancer cell lines (HCT‐15, LoVo, DLD‐1, CoLo201) was studied. In agreement with histopathologic monitoring, these tumor cells were found to produce gal‐3, while only CoLo201 was positive for gal‐1. Except for DLD‐1 and gal‐1, the lines exhibited gal‐1 binding sites on the surface, prompting study by computer‐assisted videomicroscopy of the effect on cell migration of the presence of galectin on the culture substrate. The level of cell migration for HCT‐15, LoVo and CoLo201 cells was significantly reduced by 0.15 μg/cm^2^ gal‐1, and the presence of a blocking antibody at least reduced this effect. gal‐3 significantly reduced cell migration in all 4 of the in vitro cell lines. © 2002 Wiley‐Liss, Inc.