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図書

図書
editor, Robert C. Gallo
出版情報: Cleveland : CRC Press, c1977
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2.

論文

論文
Ichimatsu, Daisuke ; Nomura, Masaaki ; Nakamura, Seiji ; Moritani, Syuzo ; Yokogawa, Koichi ; Kobayashi, Shinjiro ; Nishioka, Tatsuo ; Miyamoto, Kenichi
出版情報: Molecular Carcinogenesis.  46  pp.436-445,  2007-06-01.  John Wiley & Sons
URL: http://hdl.handle.net/2297/6749
概要: 金沢大学医学部附属病院薬剤部<br />We found that quercetin, myricetin, quercetagetin, fisetin, (-)-epigallocatechin gallate (EGCG ), and theaflavins, among 24 flavonoids examined, markedly inhibited epidermal growth factor (EGF)-induced cell transformation of mouse epidermal JB6 Cl 41 cells. The six flavonoids suppressed the EGF-induced activation of activator protein 1 (AP-1). In addition, myricetin, quercetagetin, EGCG, and theaflavins directly inhibited EGF-induced phosphatidylinositol 3-kinase (PI3K) activation. The important structural features of flavonoids for cell transformation-inhibitory activity are 3′- and 4′-OH on the B-ring, 3-OH on the C-ring, C2=C3 double bond in the C-ring, and the phenylchromone (C6-C5-C6) skeleton in the flavonols, and the galloyl group in EGCG and theaflavins. Our results provide new insight into possible mechanisms of the anti-carcinogenic effects of flavonoids, and could help to provide a basis for the design of novel cancer chemopreventive agents. © 2007 Wiley-Liss, Inc. 続きを見る
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論文

論文
Nomura, Masaaki ; Ichimatsu, Daisuke ; Moritani, Shuzo ; Koyama, Ichiko ; Dong, Zigang ; Yokogawa, Koichi ; Miyamoto, Kenichi
出版情報: Molecular Carcinogenesis.  44  pp.67-76,  2005-09-01.  Wiley-Liss
URL: http://hdl.handle.net/2297/6720
概要: 金沢大学医学部附属病院薬剤部<br />We found that caffeine significantly inhibited epidermal growth factor (EGF)- and 12-O-tetrade canoylphorbol-13-acetate (TPA)-induced cell transformation in the JB6 mouse epidermal cell line. The tumor promoter-induced cell transformation was also blocked by treatment with an adenosine A1 receptor antagonist, 8-phenyltheophylline (8-PTH). Caffeine slightly attenuated activation of EGF-induced activator protein 1 (AP-1) activation, which play important roles in cell transformation, but only at the highest concentration examined (1 mM). Interestingly, pretreatment with caffeine suppressed EGF-induced phosphorylation and activation of Akt and ribosomal p70 S6 protein kinase (p70 S6K), a target of Akt, without inhibiting phosphatidylinositol 3-kinase (PI3K) activation. The inhibition of Akt activation of caffeine was not a result of its adenosine receptor antagonism. Because Akt plays a key role in signal transduction pathways leading to cell proliferation and apoptosis, our results provide novel insight into possible mechanisms of the chemotherapeutic effect of caffeine. © 2005 Wiley-Liss, Inc. 続きを見る
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論文

論文
Nomura, Masaaki ; He, Zhiwei ; Koyama, Ichiko ; Ma, Wei-Ya ; Miyamoto, Kenichi ; Dong, Zigang
出版情報: Molecular Carcinogenesis.  38  pp.25-32,  2003-09-01.  Wiley-Liss
URL: http://hdl.handle.net/2297/6721
概要: 金沢大学医学部附属病院薬剤部<br />Our previous study demonstrated that phosphatidylinositol 3-kinase (P13K) is necessary for epi dermal growth factor (EGF)-induced cell transformation in mouse epidermal JB6 cells. Akt and the mammalian target of rapamycin (mTOR) are regarded as P13K downstream effectors. Therefore, in this study, we investigated the role of Akt and mTOR on EGF-induced cell transformation in JB6 cells using rapamycin, a specific mTOR inhibitor, and cells expressing dominant negative mutants of Akt1 (DNM-Akt1). We found that the treatment of cells with rapamycin inhibited EGF-induced cell transformation but only slightly inhibited JB6 cell proliferation at 72 h. Although LY294002, a P13K inhibitor, attenuated EGF-induced activator protein 1 (AP-1) activation, treatment with rapamycin did not affect AP-1 activity. Treatment with rapamycin inhibited EGF-induced phosphorylation and activation of ribosomal p70 S6 protein kinase (p70 S6K), an mTOR downstream target, but had no effect on phosphorylation and activation of Akt. Rapamycin also had no effect on EGF-induced phosphorylation of extracellular signal-regulated protein kinases (ERKs). We showed that introduction of DNM-Akt1 into JB6 mouse epidermal Cl 41 (JB6 Cl 41) cells inhibits EGF-induced cell transformation without blocking cell proliferation. The expression of DNM-Akt1 also suppressed EGF-induced p70 S6K activation as well as Akt activation. These results indicated an involvement of the Akt/mTOR pathway in EGF-induced cell transformation in JB6 cells. © 2005 Wiley-Liss, Inc. 続きを見る