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Celastrol causes apoptosis and cell cycle arrest in rat glioma cells

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机构: [1]Department of Neurosurgery, First Hospital of Jilin University, Changchun 130021China [2]Department of Neurosurgery, Xuanwu Hospital of Capital University of Medical Science, Beijing 10053, China [3]Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA [4]Division of Cancer Genetics, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo 102-8251, Japan
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关键词: Celastrol apoptosis cell cycle proteasome glioma

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Glioma still remains a major health problem in the world. Celastrol has been proved to be an effective natural proteasome inhibitor and was used for treatment of autoimmune disease, chronic inflammation and neurodegenerative disease. However, its effect on glioma is unclear. In this study, we investigated the therapeutic effects of celastrol on C6 glioma cells. The results demonstrated that celastrol inhibited cell proliferation in a time-and dose-dependent manner, suppressed proteasome chymotrypsin-like activity and induced apoptosis and cell cycle arrest at G2/M phase in C6 cells. Proapoptosis proteins bax and caspase-3 were up-regulated, as well as cell cycle G2/M-related proteins cyclin B-1, p21 and p27. Conversely, anti-apoptosis proteins bcl-2 and XIAP and cell cycle regulator cyclin-dependent kinase 2 were down-regulated. Taken together, our data suggest that celastrol can suppress proteasome activity and induce apoptosis and cell cycle arrest in C6 glioma cells, which make it be a potential drug for glioma.

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出版当年[2009]版:
大类 | 4 区 医学
小类 | 4 区 临床神经病学 4 区 神经科学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 临床神经病学 4 区 神经科学
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出版当年[2008]版:
Q3 CLINICAL NEUROLOGY Q4 NEUROSCIENCES
最新[2023]版:
Q3 CLINICAL NEUROLOGY Q4 NEUROSCIENCES

影响因子: 最新[2023版] 最新五年平均 出版当年[2008版] 出版当年五年平均 出版前一年[2007版] 出版后一年[2009版]

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第一作者机构: [1]Department of Neurosurgery, First Hospital of Jilin University, Changchun 130021China
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通讯机构: [1]Department of Neurosurgery, First Hospital of Jilin University, Changchun 130021China
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