S. Taga et al., DIFFERENTIAL REGULATION OF GLYCOSPHINGOLIPID BIOSYNTHESIS IN PHENOTYPICALLY DISTINCT BURKITTS-LYMPHOMA CELL-LINES, International journal of cancer, 61(2), 1995, pp. 261-267
Earlier studies have shown that Burkitt's lymphoma (BL) cell lines can
be divided into 2 major groups: group I, which retain the original BL
biopsy phenotype with expression of CD10 and CD77 antigens and lack o
f B-cell activation markers, and group III, which, after several in vi
tro passages, progress toward an ''LCL-like'' phenotype with loss of C
D10 and CD77 expression and up-regulation of B-cell activation antigen
s. In previous studies we have shown that several glycolipid molecules
constitute stage-specific antigens for B cells and that sequential sh
ifts in the 3 major glycolipid series ave observed during B-cell diffe
rentiation, these changes being mostly due to sequential activations o
f the corresponding glycosyltransferases. In the present work, 10 BL c
ell lines with group I or group III phenotype have been examined for c
ell surface expression of 5 glycolipid antigens (LacCer, GM3, Gb3/CD77
, Gb4 and GM2), total glycolipid content and enzymatic activities of 4
glycosyltransferases (GM3, Gb3, Gb4 and GM2 synthetases). We now repo
rt that group I and group III BL cells differ in their glycolipid meta
bolism and express either mostly globoseries or ganglioseries compound
s. Indeed, Gb3 is the major glycolipid of group I cells, whereas GM3 a
nd GM2 are the 2 major components of group III cells, and these phenot
ypic differences are mainly due to differential activities of the corr
esponding glycosyltransferases: group I cells have high Gb3 synthetase
activities and low or no GM3 and GM2 synthetase activities, whereas g
roup III cells have high GM3 and GM2 synthetase activities and low Gb3
synthetase activities. Finally, we also show that, unlike LCL, group
III BL cells do not synthesize Gb4. (C) 1995 Wiley-Liss, Inc.