title: Different patterns of glycolipid antigens are expressed following differentiation of TERA-2 human embryonal carcinoma cells induced by retinoic acid, hexamethylene bisacetamide (HMBA) or bromodeoxyuridine (BUdR).
abstract: NTERA-2 cl.D1 human embryonal carcinoma (EC) cells were induced to differentiate by either bromodeoxyuridine (BUdR) or hexamethylene bisacetamide (HMBA), and also by retinoic acid. Following exposure to each of these inducers, the globoseries glycolipid antigens stage-specific embryonic antigens -3 and -4 (SSEA-3 and -4) and the glycoprotein antigen TRA-1-60, all characteristic of the human EC cell surface, underwent a marked reduction in expression within about 7 days. At the same time, the lactoseries glycolipid antigen SSEA-1, and ganglioseries antigens A2B5 (GT3) and ME311 (9-0-acetyl GD3) were induced in BUdR- and retinoic acid-treated cells. However, these antigens did not appear during the first 7-14 days of HMBA-induced differentiation. The observations of cell surface antigen expression were paralleled by analysis of glycolipids isolated from the cells by thin-layer chromatography. This analysis, in which the new monoclonal antibodies VINIS-56 and VIN-2PB-22 were included, also revealed expression of gangliosides GD3 and GD2 in all differentiated cultures, albeit at much lower levels following HMBA exposure than following retinoic acid or BUdR-exposure. Further, disialylparagloboside was detected in retinoic acid and BUdR-induced, but not HMBA-induced, cultures. Taken with morphological observations, the results suggest that HMBA induces differentiation of NTERA-2 cl.D1 EC cells along a pathway distinct from the pathway(s) induced by retinoic acid and BUdR.
authors.affiliation: Wistar Institute of Anatomy and Biology, Philadelphia, PA 19104.
authors.forename: P W
authors.initials: PW
authors.lastname: Andrews
authors.forename: E
authors.initials: E
authors.lastname: Nudelman
authors.forename: S
authors.initials: S
authors.lastname: Hakomori
authors.forename: B A
authors.initials: BA
authors.lastname: Fenderson
mesh_terms: D000081:Acetamides / Q000494:pharmacology*; D000911:Antibodies, Monoclonal / Q000276:immunology; D000918:Antibody Specificity; D000951:Antigens, Neoplasm / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D000954:Antigens, Surface / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D014408:Biomarkers, Tumor / Q000276:immunology; D001973:Bromodeoxyuridine / Q000494:pharmacology*; D002462:Cell Membrane / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D002471:Cell Transformation, Neoplastic / Q000187:drug effects / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D006017:Glycolipids / Q000276:immunology*; D006801:Humans; D008563:Membrane Lipids / Q000378:metabolism; D012176:Retinoids / Q000494:pharmacology*; D013724:Teratoma / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D014407:Tumor Cells, Cultured / Q000276:immunology / Q000378:metabolism / Q000473:pathology
chemical_list: D000081:Acetamides; D000911:Antibodies, Monoclonal; D000951:Antigens, Neoplasm; D000954:Antigens, Surface; D014408:Biomarkers, Tumor; D006017:Glycolipids; D008563:Membrane Lipids; D012176:Retinoids; D001973:Bromodeoxyuridine; C014026:hexamethylene bisacetamide