Low complex ganglioside expression characterizes human neuroblastoma cell lines.
Low (< or = 35%) or absent expression of the complex 'b' pathway gangliosides GD1b, GT1b and GQ1b (CbG) correlates with an aggressive biological phenotype in human neuroblastoma tumors. To develop an in vitro model to probe mechanisms by which CbG may contribute to neuroblastoma behavior, we have comprehensively evaluated ganglioside expression in nine well-established human neuroblastoma cell lines, all derived from poor prognosis tumors. Total cellular ganglioside content ranged from 8 to 69 nmol/10(8) cells. High performance thin layer chromatography revealed that the simple disialoganglioside GD2 was prominent in eight of the cell lines (up to 60% of total gangliosides), whereas CbG were low (1-21%) in all nine cell lines. The structurally most complex 'b' pathway species, GQ1b, was not detected in any of the cell lines. The prominence of GD2 in neuroblastoma cell lines mirrors the high expression of GD2 that characterizes human neuroblastoma tumors, and the low CbG expression in the cell lines is analogous to that found in clinically and biologically unfavorable neuroblastoma tumors, thus establishing these neuroblastoma cell lines as valuable model systems for study of the role of CbG in the pathobiology of human neuroblastoma.
Hettmer
Simone
S
Glycobiology Program, Center for Cancer and Immunology Research, Children's National Medical Center, Children's Research Institute, Department of Pediatrics, George Washington University School of Medicine and Health Sciences, Washington DC 20010, USA.
Ladisch
Stephan
S
Kaucic
Karen
K
D002470:Cell Survival; D002855:Chromatography, Thin Layer; D005732:Gangliosides / Q000096:biosynthesis* / Q000235:genetics; D020869:Gene Expression Profiling; D006801:Humans; D009447:Neuroblastoma / Q000235:genetics* / Q000473:pathology*; D010641:Phenotype; D011379:Prognosis; D014407:Tumor Cells, Cultured
D005732:Gangliosides; C033851:ganglioside, GD1b; C016481:trisialoganglioside GT1; C039129:GQ1b ganglioside