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The apoptosis-resistance in t-AUCB-treated glioblastoma cells depends on activation of Hsp27

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机构: [1]Department of Neurosurgery, Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou 215004, Jiangsu, China [2]Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China
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关键词: Soluble epoxide hydrolase Inhibitor Glioma Chemotherapy Resistance Heat shock protein 27

摘要:
We previously reported that sEH inhibitor t-AUCB suppresses the growth of human glioblastoma U251 and U87 cell lines and induces cell-cycle G0/G1 phase arrest. In present study, we found even 96 h-treatment of 200 mu M t-AUCB can not induce apoptosis in U251 and U87 cells. We also revealed that 200 mu Mt-AUCB significantly elevates the activation of p38 MAPK, MAPKAPK2 and Hsp27. The p38 MAPK inhibitor SB203580 and the inhibitor of Hsp27 phosphorylation, KRIBB3, were used to investigate the mechanism of the apoptosis-resistance. The results showed that, after blocking the activation of Hsp27 by SB203580 or KRIBB3, 200 mu M t-AUCB significantly induces apoptosis and increases caspase-3 activities in U251 and U87 cells. Our data demonstrated that t-AUCB induces cell apoptosis after blocking itself-induced activation of Hsp27, and that the activation of Hsp27 may confer chemoresistance in GBM cells. The combination of t-AUCBand the inhibitor of Hsp27 phosphorylation may be a potential strategy for treatment of glioblastoma.

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出版当年[2011]版:
大类 | 3 区 医学
小类 | 3 区 临床神经病学 3 区 肿瘤学
最新[2023]版:
大类 | 2 区 医学
小类 | 3 区 临床神经病学 3 区 肿瘤学
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出版当年[2010]版:
Q2 ONCOLOGY Q2 CLINICAL NEUROLOGY
最新[2023]版:
Q2 CLINICAL NEUROLOGY Q2 ONCOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2010版] 出版当年五年平均 出版前一年[2009版] 出版后一年[2011版]

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第一作者机构: [1]Department of Neurosurgery, Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou 215004, Jiangsu, China
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通讯机构: [1]Department of Neurosurgery, Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou 215004, Jiangsu, China
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