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Two polychlorinated hydrocarbons cause phospholipid‐dependent protein kinase C activation in vitro in the absence of calcium
Author(s) -
Rotenberg Susan A.,
Weinstein I. Bernard
Publication year - 1991
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940040611
Subject(s) - biology , in vitro , phospholipid , calcium , microbiology and biotechnology , biochemistry , kinase , protein kinase a , medicine , membrane
Polychlorinated hydrocarbons known to be nongenotoxic carcinogens were screened as activators of protein kinase C (PKC)‐β1 either at high concentrations of Ca 2+ or in the absence of Ca 2+ (i.e., with 1 mM ethylene glycol‐ bis (β‐aminoethyl ether) N , N , N ′, N ′,‐tetraacetic acid). Of those compounds tested, kepone and dicofol significantly stimulated PKC activity in the absence, but not the presence, of Ca 2+ . PKC activation was most pronounced in the presence of phosphatidylserine. Kepone and dicofol stimulated PKC activity 26% and 13%, respectively, as compared with the PKC activity (100%) stimulated by the tumor‐promoting phorbol ester 12‐ O ‐tetradecanoylphorbol‐13‐acetate (TPA). Northern blot analysis of expression of TPA‐inducible genes by kepone showed slight expression of phorbin and ornithine decarboxylase in murine embryo fibroblasts. Future studies are required to determine the relevance of PKC activation by kepone and dicofol to the known carcinogenicity of these compounds.