Riede E, Gratchev A, Foss H D, Mann B, Buhr H J, Hanski C
Abteilung für Allgemein-, Gefäss- und Thoraxchirurgie, Universitätsklinikum Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin.
Langenbecks Arch Chir Suppl Kongressbd. 1998;115(Suppl I):299-302.
MUC2 is known to be the main intestinal mucin carrying the carbohydrate moiety sialyl-Le(x), which interacts with the endothelial molecule E-selectin. This interaction may contribute to the extravasation of tumor cells and thus to the metastatic process. We analysed MUC2 expression in normal colonic, carcinomatous and metastatic tissue and the regulation of MUC2 gene expression. In metastases MUC2 expression was significantly lower than in normal tissue and primary tumors and seems not to be related to the metastatic process. In several colorectal carcinoma cell lines the methylation of the 5'-flanking region of MUC2 correlated with the suppression of the MUC2 gene. The increase of the MUC2 expression after the inhibition of the methylation with 5-aza-2' deoxycytidine strongly support the notion that the suppression of MUC2 gene is causally related to the methylation of the promoter.
已知MUC2是携带碳水化合物部分唾液酸化刘易斯x(sialyl-Le(x))的主要肠道黏蛋白,其与内皮分子E-选择素相互作用。这种相互作用可能有助于肿瘤细胞的外渗,进而促进转移过程。我们分析了MUC2在正常结肠、癌组织和转移组织中的表达以及MUC2基因表达的调控。在转移灶中,MUC2的表达显著低于正常组织和原发性肿瘤,且似乎与转移过程无关。在几种结肠癌细胞系中,MUC2 5'-侧翼区域的甲基化与MUC2基因的抑制相关。用5-氮杂-2'-脱氧胞苷抑制甲基化后MUC2表达的增加有力地支持了MUC2基因的抑制与启动子甲基化存在因果关系这一观点。