Roles of SIRT1 and Phosphoinositide 3-OH Kinase/Protein Kinase C Pathways in Evodiamine-Induced Human Melanoma A375-S2 Cell Death
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- Wang Che
- China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University Department of Pharmacology, Shenyang Pharmaceutical University
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- Wang Min-wei
- Department of Pharmacology, Shenyang Pharmaceutical University
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- Tashiro Shin-ichi
- Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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- Onodera Satoshi
- Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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- Ikejima Takashi
- China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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説明
We previously demonstrated that evodimine isolated from Evodia rutaecarpa (Goshuyu in Japan) induced apoptosis in human malignant melanoma A375-S2 cells within 24 h. In this study, TUNEL assay also indicated that one cause of A375-S2 cell death induced by evodiamine was apoptosis. After treatment with evodiamine for the indicated time periods, anti-apoptotic protein SIRT1 expression was decreased; p53 expression and its phosphorylation were both enhanced, whereas transient induction of downstream p21 was not enough to promote cell cycle arrest. Inhibition of the phosphoinositide 3-OH kinase (PI3-K)/protein kinase C (PKC) survival pathway as well as subsequent inhibition of the ERK cascade might contribute to evodiamine-induced cell death. In addition, p53 activation in response to evodiamine administration was correlated with the activation of the PI3-K/PKC pro-apoptotic pathway, but did not require ERK participation. The inhibition of the PI3-K/PKC survival pathway might be responsible for SIRT1 inactivation and increased Bax/Bcl-2 expression ratio in evodiamine-induced cell death.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 97 (4), 494-500, 2005
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680152588672
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- NII論文ID
- 10025727457
- 30003473090
- 130000074330
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7301005
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- PubMed
- 15821341
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- 本文言語コード
- en
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- データソース種別
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