Activation of hypoxia signaling induces phenotypic transformation of glioma cells: implications for bevacizumab antiangiogenic therapy
文献类型：期刊论文
| 作者 | Xu, Hui1; Rahimpour, Shervin2; Nesvick, Cody L.2; Zhang, Xu1; Ma, Jingyun1; Zhang, Min1; Zhang, Ge3; Wang, Li1; Yang, Chunzhang2; Hong, Christopher S.2 |
| 刊名 | oncotarget
 |
| 出版日期 | 2015-05-20 |
| 卷号 | 6期号:14页码:11882-11893 |
| 关键词 | glioblastoma bevacizumab epithelial-mesenchymal transition pathologic angiogenesis hypoxia-inducible factor |
| 英文摘要 | glioblastoma (gbm) is the most common and deadly primary brain tumor in adults. bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (vegf), can attenuate tumor-associated edema and improve patient symptoms but based on magnetic resonance imaging, is associated with non-enhancing tumor progression and possibly gliosarcoma differentiation. to gain insight into these findings, we investigated the role of hypoxia and epithelial-mesenchymal transition (emt)-associated proteins in gbm. tumor markers of hypoxia and emt were upregulated in bevacizumab-treated tumors from gbm patients compared to untreated counterparts. exposure of glioma cells to 1% oxygen tension increased cell proliferation, expression of emt-associated proteins and enhanced cell migration in vitro. these phenotypic changes were significantly attenuated by pharmacologic knockdown of hypoxia-inducible factor 1 alpha (hif1 alpha) or hif2 alpha, indicating that hifs represent a therapeutic target for mesenchymal gbm cells. these findings provide insights into potential development of novel therapeutic targeting of angiogenesis-specific pathways in gbm. |
| WOS标题词 | science & technology ; life sciences & biomedicine |
| 类目[WOS] | oncology ; cell biology |
| 研究领域[WOS] | oncology ; cell biology |
| 关键词[WOS] | endothelial growth-factor ; epithelial-mesenchymal transition ; recurrent malignant glioma ; receptor inhibitor su5416 ; anti-angiogenic therapy ; inducible factor-i ; stem-cells ; phase-ii ; glioblastoma-multiforme ; tumor progression |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000359008200013 |
| 公开日期 | 2016-05-09 |
| 源URL | [http://cas-ir.dicp.ac.cn/handle/321008/146438]  |
| 专题 | 大连化学物理研究所_中国科学院大连化学物理研究所 |
| 作者单位 | 1.Chinese Acad Sci, Dalian Inst Chem Phys, Div Biotechnol, Dalian, Peoples R China 2.NINDS, Surg Neurol Branch, Bethesda, MD 20892 USA 3.Dalian Med Univ, Dept Immunol, Dalian, Peoples R China 4.Loyola Univ, Med Ctr, Dept Neurol Surg, Chicago, IL 60611 USA 5.Ohio State Univ, Med Ctr, Dept Neurol Surg, Columbus, OH 43210 USA 6.Fudan Univ, Dept Neurosurg, Huashan Hosp, Shanghai Med Coll, Shanghai 200433, Peoples R China 7.Univ Texas MD Anderson Canc Ctr, Dept Neuro Oncol, Div Canc Med, Houston, TX 77030 USA |
| 推荐引用方式 GB/T 7714 | Xu, Hui,Rahimpour, Shervin,Nesvick, Cody L.,et al. Activation of hypoxia signaling induces phenotypic transformation of glioma cells: implications for bevacizumab antiangiogenic therapy[J]. oncotarget,2015,6(14):11882-11893. |
| APA | Xu, Hui.,Rahimpour, Shervin.,Nesvick, Cody L..,Zhang, Xu.,Ma, Jingyun.,...&Zhuang, Zhengping.(2015).Activation of hypoxia signaling induces phenotypic transformation of glioma cells: implications for bevacizumab antiangiogenic therapy.oncotarget,6(14),11882-11893. |
| MLA | Xu, Hui,et al."Activation of hypoxia signaling induces phenotypic transformation of glioma cells: implications for bevacizumab antiangiogenic therapy".oncotarget 6.14(2015):11882-11893. |
入库方式： OAI收割
来源：大连化学物理研究所
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