マウス大腸がん細胞およびマウスメラノーマ細胞の遊走能に及ぼす炎症性刺激の影響

We previously reported that inflammatory stimulation reduced the tumor suppressor gene Programmed cell death 4 (Pdcd4) protein expression level and enhanced the metastatic abilityof human colon cancer cells. In this study, we investigated the effect of 12-O-tetradecanoylphorbol 13-acetate (TPA) stim...

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Bibliographic Details
Published in日本薬理学会年会要旨集 p. 1-P-097
Main Authors 菅野, 莉央, 図子, 菜月, 吉川, 紀子, 岩田, 恵理子, 畑井, 麻友子, 籠田, 智美, 篠塚, 和正, 中村, 一基
Format Journal Article
LanguageJapanese
Published 公益社団法人 日本薬理学会 2019
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Summary:We previously reported that inflammatory stimulation reduced the tumor suppressor gene Programmed cell death 4 (Pdcd4) protein expression level and enhanced the metastatic abilityof human colon cancer cells. In this study, we investigated the effect of 12-O-tetradecanoylphorbol 13-acetate (TPA) stimulation on the expression levels of Pdcd4 protein and migratory ability in mouse Colon-26 cancer cells and B16-BL6 melanoma cells.The expression level of Pdcd4 protein in Colon-26 cells treated with TPA significantly decreased in a concentration-dependent manner. On the other hand, Pdcd4 protein in B16-BL6 cells treated with TPA significantly increased in a concentration-dependent manner. In addition, the migratory ability of Colon-26 cells treated with TPA were significantly increased, but the migration of B16-BL6 cells treated with TPA were significantly decreased. Furthermore, we measured the melanin content of the cells and tyrosinase activity as indices of activation of Protein Kinase C (PKC). The melanin content and tyrosinase activity were significantly decreased in B16-BL6 cells treated with TPA.These results indicated that Pdcd4 might be a negative regulator in the migratory ability of Colon-26 and B16-BL6 cells. Although the activation of PKC promoted degradation of Pdcd4 in Colon-26 cells, it did not function in B16-BL6 cells.
Bibliography:92_1-P-097
ISSN:2435-4953
DOI:10.1254/jpssuppl.92.0_1-P-097