DICP OpenIR
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
KeywordGlioblastoma Bevacizumab Epithelial-mesenchymal Transition Pathologic Angiogenesis Hypoxia-inducible Factor
Source PublicationONCOTARGET
2015-05-20
Volume6Issue:14Pages:11882-11893
Indexed BySCI
SubtypeArticle
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
WOS SubjectOncology ; Cell Biology
WOS Research AreaOncology ; Cell Biology
WOS KeywordENDOTHELIAL 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
AbstractGlioblastoma (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.
Language英语
WOS IDWOS:000359008200013
Citation statistics
Cited Times:37[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://cas-ir.dicp.ac.cn/handle/321008/146438
Collection中国科学院大连化学物理研究所
Affiliation1.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
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.
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