A and H blood group antigens as markers of sucrase-isomaltase from the enterocyte-like differentiated human colon carcinoma cell lines HT-29 and Caco-2.

The purpose of this work was to investigate whether sucrase-isomaltase from enterocyte-like differentiated human colon carcinoma cell lines carries blood group antigens of the ABH system. Six cultured lines of blood group A (HT-29, SW-480, Co-115) or O phenotype (Caco-2, HRT-18, HCT-8R) were studied. Only HT-29 cells grown in the absence of glucose (HT-29 Glc-) and Caco-2 cells express an enterocytic differentiation with the presence of sucrase-isomaltase on the apical surface of the cells. Binding of anti-A antibodies to HT-29 Glc- and of UEA-I to Caco-2 cells gave the same apical immunofluorescence pattern of staining as did anti-sucrase-isomaltase antibodies, whereas only a membrane binding was observed in nondifferentiated cells. Sucrase-isomaltase immunoisolated from HT-29 Glc- and Caco-2 cells reacted with anti-A antibodies and Ulex europaeus agglutinin-I (UEA-I), respectively, at sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblot. Immunoprecipitation of solubilized brush border-enriched fractions from the same cells with UEA-I or anti-A antibodies resulted in an inhibition of sucrase activity which reached congruent to 80% for Caco-2 cells with UEA-I and approximately equal to 50% for HT-29 cells with anti-A antibodies. Similar results were obtained in the corresponding tumors in nude mice: anti-A antibodies in HT-29 and UEA-I in Caco-2 tumors bound to the same apical structures as did anti-sucrase-isomaltase antibodies; sucrase-isomaltase immunoisolated from the tumors bound anti-A antibodies (HT-29) or UEA-I (Caco-2). These results support the hypothesis that sucrase-isomaltase from enterocyte-like differentiated human colon cancer cells carries blood group antigens of the ABH system. These findings suggest that colon cancers which have been shown to display an apical pattern of expression of ABH antigens should be screened for their possible enterocytic differentiation.