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Induction of the fundic mucosa‐specific glycolipid with dimethylformamide in gastric‐cancer cell lines
Author(s) -
Dohi Taeko,
Nakasuji Miyuki,
Oshima Mieko
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910530125
Subject(s) - glycolipid , gastric mucosa , cancer , dimethylformamide , medicine , cancer research , pathology , biology , stomach , immunology , biochemistry , solvent
Abstract We have previously reported that a glycolipid GalNAcβ I‐4[NeuAcα2‐3]Galβ I‐4GlcNAcβ I ‐3Galβ I‐4Glc‐Cer named NGM‐I is present specifically in the human gastric fundic mucosa, but not in other organs. In gastric‐cancer tissue and cancer cell lines, this glycolipid completely disappears. These findings imply that NGM‐I is expressed only in well‐differentiated fundic mucosa. The purpose of this study is to examine the expression of NGM‐I as a differentiation‐related molecule. A gastric cell line AZ52I was cultured in the medium with various reagents which had been reported to induce differentiation in cancer cells. The growth of AZ52I was suppressed by the addition of 0.8% dimethylformamide (DMF) to the medium, but not by addition of dimethylsulfoxide (DMSO), retinoic acid or butyric acid. In the ganglioside fraction of the cells cultured with DMF. a glycolipid regarded as NGM‐I which had not been present before treatment was detected using a monoclonal antibody. Suppression of the proliferation of AZ52I by eliminating the serum from the medium could not induce the expression of NGM‐I. A colonic cell line treated with DMF also failed to express the glycolipid. The synthase activity of NGM‐I was elevated in the AZ52I cells treated with DMF, but not with DMSO. These results demonstrate that the expression of NGM‐I is induced by DMF specifically in gastric‐cancer cells, and suggest the possibility that NGM‐I is a differentiation‐related molecule.