Effect of glucocorticoids on TPA-induced inhibition of gap-junctional communication and morphological transformation in Syrian hamster embryo cells.
The effect of glucocorticoids on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced inhibition of gap-junctional intercellular communication (GJIC) and morphological transformation in Syrian hamster embryo (SHE) cells was examined. Fluocinolone acetonide (FA) and dexamethasone (DEX) almost completely suppressed the effect of TPA on induction of transformed morphology. On the other hand, up to 1000 times higher FA and DEX concentrations did not influence the inhibitory effect of TPA on GJIC. Neither treatment with these glucocorticoids for 4, 24 or 48 h before TPA exposure nor 24 h co-exposure with TPA altered the effect of TPA on GJIC. Thus the potent effect of glucocorticoids as inhibitors of the promotional effect of TPA on morphological transformation in SHE cells does not result in alterations of TPA-induced inhibition of GJIC.
Roseng
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LE
Laboratory for Environmental and Occupational Cancer, Norwegian Radium Hospital, Oslo.
Rivedal
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D000818:Animals; D002450:Cell Communication / Q000187:drug effects*; D002471:Cell Transformation, Neoplastic / Q000187:drug effects*; D002478:Cells, Cultured; D006224:Cricetinae; D004622:Embryo, Mammalian / Q000166:cytology / Q000187:drug effects*; D017629:Gap Junctions / Q000187:drug effects*; D005938:Glucocorticoids / Q000494:pharmacology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D005938:Glucocorticoids; D013755:Tetradecanoylphorbol Acetate