Adhesion defect of ascites cells corrected with membrane-bound attachment molecules.
Adhesion is obligatory for cell proliferation in most types of cells. This function becomes defective after malignant transformation. An extreme example is ascites cells which proliferate in suspension. The nature of their defects remains obscure. Here we show that the linking of biotin molecules to the Ehrlich ascites carcinoma cells enables these cells to spread normally on an avidin-coated substrate. The spreading was the result of specific avidin-biotin interaction. The morphology of the spread cells and sensitivity to different inhibitors are similar to those of normal epithelia. Thus it is enough to supply appropriate substrate-adhesive molecules to the ascites cell surface to normalize their adhesion.
Gordeeva
L V
LV
Belozersky Laboratory of Molecular Biology and Bio-Organic Chemistry, Moscow State University, USSR.
Bogdanov
A A
AA
Baibakov
B A
BA
Torchilin
V P
VP
Margolis
L B
LB
D000818:Animals; D000954:Antigens, Surface; D001710:Biotin; D002286:Carcinoma, Ehrlich Tumor / Q000473:pathology* / Q000648:ultrastructure; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules; D002462:Cell Membrane / Q000648:ultrastructure; D051379:Mice; D008855:Microscopy, Electron, Scanning
D000954:Antigens, Surface; D015815:Cell Adhesion Molecules; D001710:Biotin