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题名: Activation of hypoxia signaling induces phenotypic transformation of glioma cells: implications for bevacizumab antiangiogenic therapy
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;  Germanwala, Anand V.4;  Elder, J. Bradley5;  Ray-Chaudhury, Abhik2;  Yao, Yu6;  Gilbert, Mark R.7;  Lonser, Russell R.5;  Heiss, John D.2;  Brady, Roscoe O.2;  Mao, Ying6;  Qin, Jianhua1;  Zhuang, Zhengping2
关键词: glioblastoma ;  bevacizumab ;  epithelial-mesenchymal transition ;  pathologic angiogenesis ;  hypoxia-inducible factor
刊名: ONCOTARGET
发表日期: 2015-05-20
卷: 6, 期:14, 页:11882-11893
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology ;  Life Sciences & Biomedicine
类目[WOS]: Oncology ;  Cell Biology
研究领域[WOS]: Oncology ;  Cell Biology
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.
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
语种: 英语
WOS记录号: WOS:000359008200013
Citation statistics: 
内容类型: 期刊论文
URI标识: http://cas-ir.dicp.ac.cn/handle/321008/146438
Appears in Collections:中国科学院大连化学物理研究所_期刊论文

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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

Recommended Citation:
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.
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