The induction of tumour cell adhesiveness and intercellular junctions by a glycoprotein of rat ascites hepatoma cell surface.
Rat ascites hepatoma AH109A cells (present as a free form in vivo) can aggregate and then develop well-defined tripartite junctional complexes, including intermediate junctions, desmosomes and focal tight junctions, on incubation with a glycoprotein separated from rat ascites hepatoma AH136B cells (forming cell islnds in vivo). The development of binding structures was strongly inhibited by actinomycin D. AH109A cells or rat ascites hepatoma YS cells (present as a free form in vivo) previously treated with the glycoprotein for 24 h, when inoculated i.p., proliferated as free cells in the ascitic fluid, like the untreated cells. AH109A cells actively proliferating in the skin do not form any junctional complexes. The reason for the failure of island formation by AH109A cells or YS cells in vivo is discussed.
D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000032:analysis* / Q000648:ultrastructure; D002448:Cell Adhesion / Q000187:drug effects*; D003115:Colony-Stimulating Factors; D003609:Dactinomycin / Q000494:pharmacology; D003896:Desmosomes / Q000648:ultrastructure; D006023:Glycoproteins / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D066298:In Vitro Techniques; D007365:Intercellular Junctions / Q000187:drug effects*; D008113:Liver Neoplasms; D008854:Microscopy, Electron; D009363:Neoplasm Proteins / Q000494:pharmacology*; D009374:Neoplasms, Experimental / Q000032:analysis; D051381:Rats; D012878:Skin Neoplasms / Q000648:ultrastructure; D013997:Time Factors
D003115:Colony-Stimulating Factors; D006023:Glycoproteins; D009363:Neoplasm Proteins; D003609:Dactinomycin