Anthralin, a Non-TPA Type Tumor Promoter, Synergistically Enhances Phorbol Ester-Caused Prostaglandin E<SUB>2</SUB> Release from Primary Cultured Mouse Epidermal Cells
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概要
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Primary cultures of mouse epidermal cells (i.e., target cells of skin tumor promotion) stimulated by 12-<I>O</I>-tetradecanoylphorbol-13-acetate (TPA) released prostaglandin E<SUB>2</SUB> within 30 min. Anthralin, a non-TPA type tumor promoter, also stimulated PGE<SUB>2</SUB> release; however, no release was detectable at least up to 4 hr after the addition of anthralin. When the cells were incubated with TPA plus anthralin, both PGE<SUB>2</SUB> and arachidonic acid release were synergistically enhanced. Other non-TPA type tumor promoters, i.e., chrysarobin, 7-bromomethylbenz[α]anthracene, benzoylperoxide, okadaic acid and palytoxin, did not potentiate the TPA-caused PGE<SUB>2</SUB> release. In protein kinase C-down regulated cells, the synergistic stimulation of PGE<SUB>2</SUB> and arachidonic acid release by TPA plus anthralin were not detected. Anthralin plus TPA-did not alter the incorporation of arachidonic acid into cellular phospholipids. Cellular cyclooxygenase activity was increased 2 hr after TPA stimulation. Anthralin-caused increase in cyclooxygenase activity was detected at 6 hr after the addition of anthralin. Cyclooxygenase activity was synergistically increased by treating the cells with TPA plus anthralin. Cycloheximide and actinomycin D inhibited the increase in cyclooxygenase activity caused by anthralin or TPA plus anthralin. These results indicate that anthralin synergistically stimulates TPA-caused PGE<SUB>2</SUB> release by synergistically increasing arachidonic acid release and cellular cyclooxygenase activity.
著者
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Kato Ryuichi
Department Of Biology Graduate School Of Science Osaka University
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Yamamoto Satoshi
Department Of Biochemistry Nagoya University School Of Medicine
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Aizu Eriko
Kyoritsu College of Pharmacy
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