Annexin A5 promotes invasion and chemoresistance to temozolomide in glioblastoma multiforme cells
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- 作者：Lei Wu (1)
Liang Yang (2)
Yu Xiong (1)
Hua Guo (1)
Xiaoli Shen (1)
Zujue Cheng (1)
Yan Zhang (1)
Ziyun Gao (1)
Xingen Zhu (1) - 关键词：Glioblastoma multiforme ; Annexin A5 ; Invasion ; Chemoresistance ; Temozolomide ; Phosphatidylinositol 3 ; kinase
- 刊名：Tumor Biology
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：35
- 期：12
- 页码：12327-12337
- 全文大小：1,147 KB
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Liang Yang (2)
Yu Xiong (1)
Hua Guo (1)
Xiaoli Shen (1)
Zujue Cheng (1)
Yan Zhang (1)
Ziyun Gao (1)
Xingen Zhu (1)
1. Department of Neurosurgery, The Second Affiliated Hospital, Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, People鈥檚 Republic of China
2. Department of Neurosurgery, The Third Xiangya Hospital, Central South University, Changsha, Hunan, People鈥檚 Republic of China - 刊物主题：Cancer Research;
- 出版者：Springer Netherlands
- ISSN：1423-0380
文摘
Glioblastoma multiforme (GBM) is the prevalent and most fatal brain tumor in adults. Invasion and a high rate of recurrence largely contribute to the poor prognosis of GBM. The current standard therapy for GBM includes surgery with maximum feasible resection, radiotherapy, and treatment with chemotherapeutic agent temozolomide. Annexin A5 reportedly promotes progression and chemoresistance in a variety of cancers. In the present study, we explored the effects of annexin A5 on GBM cell invasion and chemoresistance to temozolomide. Stable overexpression and knockdown of annexin A5 were performed in both U-87 MG and U-118 MG human GBM cell lines. Overexpression of annexin A5 in both cell lines significantly increased cell invasion, matrix metalloproteinase-2 (MMP-2) expression/activity, Akt phosphorylation at serine 473, and the half maximal inhibitory concentration (IC50) values of temozolomide and markedly decreased temozolomide-induced apoptosis, all of which were abolished by selective PI3K inhibitor BKM120. On the other hand, knockdown of annexin A5 markedly decreased cell invasion, MMP-2 expression/activity, Akt phosphorylation at serine 473, and the IC50 values of temozolomide and significantly increased temozolomide-induced apoptosis. In conclusion, our study provides the first evidence that annexin A5 promotes GBM cell invasion, MMP-2 expression/activity, and chemoresistance to temozolomide through a PI3K-dependent mechanism. It adds new insights not only into the biological function of annexin A5 but also into the molecular mechanisms underlying GBM progression and chemoresistance.