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Activation of hypoxia signaling induces phenotypic transformation of glioma cells: implications for bevacizumab antiangiogenic therapy
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
2015-05-20
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
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
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.
语种英语
WOS记录号WOS:000359008200013
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被引频次:31[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://cas-ir.dicp.ac.cn/handle/321008/146438
专题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
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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.
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