Expression of ?2,6-sialic acid-containing and Lewis-active glycolipids in several types of human ovarian carcinomas.
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ABSTRACT: To identify glycolipid antigens associated with histologically defined types of ovarian carcinomas, we determined the amounts of ?2,6-sialyl and Lewis-active glycolipids, the specific activities of the ?2,3- and ?2,6-sialyltransferases, and the gene expression of sugar transferases in mucinous and serous cystadenocarcinoma, clear cell adenocarcinoma and endometrioid carcinoma tissues and cell lines derived from them. ?2,6-sialyl glycolipid IV(6)NeuAc?-nLc(4)Cer detected with a newly developed monoclonal antibody, Y916, was present in 5/7 serous cystadenocarcinoma cases in relatively higher amounts than those in the other carcinoma tissues. On the other hand, the amounts of Lewis-active glycolipids in serous cystadenocarcinoma tissues were lower than those in the other carcinoma tissues. No correlation was observed between the structures of Lewis glycolipids and the histological classification. The gene expression of ?2,3- and ?2,6-sialyltransferases and ?1,3/4-fucosyltransferase for the synthesis of Lewis-active glycolipids was not positively correlated with the amounts of the respective glycolipids, probably due to the epigenetic regulation of transferases in the overall metabolic pathways for lacto-series glycolipids. However, the amounts of GM3 and GD3 with short carbohydrate chains correlated with the relative intensities of GM3 and GD3 synthase gene expression, respectively. Among ovarian carcinoma-derived cell lines, the serous cystadenocarcinoma-derived ones exhibited a lower frequency of Lewis-active glycolipid expression than the other carcinoma-derived ones, which was similar to that in the respective tissues. Thus, malignancy-related Lewis-active glycolipids were shown to be regulated in different modes in ovarian serous cystadenocarcinomas and the other carcinomas.
SUBMITTER: Tanaka K
PROVIDER: S-EPMC3412467 | biostudies-literature | 2010 Nov
REPOSITORIES: biostudies-literature
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