Resveratrol-induced cell growth inhibition and apoptosis is associated with modulation of phosphoglycerate mutase B in human prostate cancer cells: two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis and mass spectrometry evaluation
Resveratrol-induced cell growth inhibition and apoptosis is associated with modulation of phosphoglycerate mutase B in human prostate cancer cells: two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis and mass spectrometry evaluation
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DOI：
10.1016/j.cdp.2004.08.009
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发表时间：
2004-01-01
影响因子：
--
通讯作者：
Nixon, DW
中科院分区：
文献类型：
--
作者：
Narayanan, NK;Narayanan, BA;Nixon, DW
一些研究提供了证据证明白藜芦醇的抗癌活性，一种存在于葡萄和浆果中的植物抗毒素，但白藜芦醇调节前列腺癌发生的确切机制仍有待阐明。白藜芦醇在人前列腺癌细胞中诱导的抑制作用影响与肿瘤发生、促进和进展相关的多种细胞机制。在我们早期使用cDNA微阵列分析前列腺癌细胞的研究中，我们指出了p53介导的白藜芦醇分子靶点的重要性。本研究的基础上，二维十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（2D-SDS-PAGE），然后用质谱分析的人前列腺细胞，已与白藜芦醇处理清楚地确定磷酸甘油酸酯β B的作用。我们首次报道了白藜芦醇处理的前列腺癌细胞LNCaP、DU 145和PC-3中磷酸甘油酸酯β B在转录水平上的表达。我们的观察提高了它对癌细胞中代谢酶的影响而不影响正常细胞的可能性。(C)2004年由Elsevier Ltd.代表国际预防肿瘤学会出版。
Several studies provide evidence for the anti-carcinogenic activity of resveratrol, a phytoalexin present in grapes and berries, but the precise mechanisms involved in the modulation of prostate carcinogenesis by resveratrol remain to be elucidated. The inhibitory effects induced by resveratrol in human prostate cancer cells impact diverse cellular mechanisms associated with tumor initiation, promotion, and progression. In our earlier studies with prostate cancer cells using cDNA microarray analysis, we indicated the importance of p53-mediated molecular targets of resveratrol. The present study based on two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis (2D-SDS-PAGE) followed by mass spectrometry analysis of human prostate cells that have been treated with resveratrol clearly identifies the role of phosphoglycerate mutase B. For the first time, we report on phosphoglycerate mutase B in the resveratrol-treated prostate cancer cells LNCaP, DU145, and PC-3 at the transcription level. Our observations raise the possibility of its effect on metabolic enzymes in cancer cells without affecting the normal cells. (C) 2004 Published by Elsevier Ltd. on behalf of International Society for Preventive Oncology.