Phorbol ester-induced anchorage independence and its antagonism by retinoic acid correlates with altered expression of specific glycoproteins.
Since tumor promoting phorbol esters produce a variety of glycoprotein synthesis changes and since retinoids act both as antipromoters and modulators of glycoprotein synthesis, we sought to ascertain whether specific changes in glycoprotein synthesis might be targets both for the promoting action of phorbol esters and for the antipromoting actin of retinoids. In this report we present evidence that tumor promoting but not nonpromoting phorbol esters produce decreased levels of 180,000 and 150,000 mol, wt, glycoproteins in mouse JB-6 cells which are promotable to tumor cell phenotype by phorbol esters. These relatively specific decreases are blocked by an antipromoting concentration of retinoic acid, thus suggesting that decreases in 180K and 150K glycoproteins may play a role in promotion of transformation.
D000818:Animals; D002273:Carcinogens / Q000037:antagonists & inhibitors / Q000633:toxicity*; D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D005786:Gene Expression Regulation / Q000187:drug effects; D006023:Glycoproteins / Q000096:biosynthesis*; D051379:Mice; D009374:Neoplasms, Experimental / Q000139:chemically induced; D010704:Phorbols / Q000037:antagonists & inhibitors / Q000633:toxicity*; D013755:Tetradecanoylphorbol Acetate / Q000037:antagonists & inhibitors / Q000633:toxicity; D014212:Tretinoin / Q000494:pharmacology*
D002273:Carcinogens; D006023:Glycoproteins; D010704:Phorbols; D014212:Tretinoin; D013755:Tetradecanoylphorbol Acetate