Retinoids induce tissue transglutaminase in NIH-3T3 cells.
We report that all-trans and 13-cis-retinoic acid as well as the synthetic compound CH-55 enhance tissue transglutaminase activity as they increase NIH-3T3 cell adhesiveness. The 4-hydroxyphenylretinamide (4-HPR) with low activity in inducing attachment, lectin binding and growth inhibition also fails to induce transglutaminase. Thyroxine (Thy), a compound with a response element common to RA, is inactive. The tumor promoter 12-tetradecanoyl-phorbol-13-acetate (TPA), which increases adhesiveness with different kinetics than RA, failed to enhance tranglutaminase. We conclude that retinoids with biological activity in inducing adhesion, inhibition of growth and increase of lectin binding, are also active in inducing transglutaminase activity.
Differentiation Control Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
D
D
Cai
T
T
Ben
L M
LM
De Luca
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D007700:Kinetics; D051379:Mice; D012176:Retinoids / Q000494:pharmacology*; D013329:Structure-Activity Relationship; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013974:Thyroxine / Q000494:pharmacology; D011503:Transglutaminases / Q000096:biosynthesis*
D012176:Retinoids; D011503:Transglutaminases; D013755:Tetradecanoylphorbol Acetate; D013974:Thyroxine