EGFR and EGFRvIII Promote Angiogenesis and Cell Invasion in Glioblastoma: Combination Therapies for an Effective Treatment.
EGFR and EGFRvIII Promote Angiogenesis and Cell Invasion in Glioblastoma: Combination Therapies for an Effective Treatment.
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DOI：
10.3390/ijms18061295
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发表时间：
2017-06-18
影响因子：
5.6
通讯作者：
Schmidt MHH
中科院分区：
文献类型：
--
作者：
Keller S;Schmidt MHH
表皮生长因子受体（EGFR）和突变型EGFRvIII是目前针对多形性胶质母细胞瘤（GBM）（最恶性的原发性脑肿瘤）的靶向癌症治疗概念中的主要焦点。该受体参与肿瘤细胞侵袭和肿瘤相关血管生成的关键过程，其上调与胶质瘤患者的不良预后相关。胶质瘤细胞侵袭和血管生成增加共享通过上调细胞外基质（ECM）降解蛋白酶以及激活异常信号传导途径而降解ECM的机制。这篇综述描述了EGFR和EGFRvIII在这些机制中的作用，这些机制可能提供新的联合治疗方法，靶向EGFR或EGFRvIII与针对ECM蛋白酶或下游信号传导的药物治疗一起，以增加单药治疗的抑制作用。
Epidermal growth factor receptor (EGFR) and the mutant EGFRvIII are major focal points in current concepts of targeted cancer therapy for glioblastoma multiforme (GBM), the most malignant primary brain tumor. The receptors participate in the key processes of tumor cell invasion and tumor-related angiogenesis and their upregulation correlates with the poor prognosis of glioma patients. Glioma cell invasion and increased angiogenesis share mechanisms of the degradation of the extracellular matrix (ECM) through upregulation of ECM-degrading proteases as well as the activation of aberrant signaling pathways. This review describes the role of EGFR and EGFRvIII in those mechanisms which might offer new combined therapeutic approaches targeting EGFR or EGFRvIII together with drug treatments against proteases of the ECM or downstream signaling to increase the inhibitory effects of mono-therapies.