缺氧诱导细胞外基质重塑在胶质瘤抗血管治疗耐药中的研究进展  

Research advances in hypoxia-induced extracellular matrix remodeling in resistance to antiangiogenic therapy in glioma

作　　者：朱陆奕 刘羽阳 陈凌 石瑛 ZHU Lu-Yi;LIU Yu-Yang;CHEN ling;SHI Ying(School of Medicine,University of Electronic Science and Technology of China,Chengdu,Sichuan 610054,China;Department of Neurosurgery,the First Medical Centre,Chinese PLA General Hospital,Beijing 100853,China)

机构地区：[1]电子科技大学医学院,四川成都610054 [2]解放军总医院第一医学中心神经外科,北京100853

出　　处：《国际神经病学神经外科学杂志》2022年第1期56-60,共5页Journal of International Neurology and Neurosurgery

摘　　要：细胞外基质(ECM)是肿瘤微环境的重要组成部分,参与调控多种肿瘤的恶性表型。在胶质瘤中,缺氧微环境可刺激细胞诱导ECM重塑,为肿瘤新生血管的形成提供空间。此外,缺氧可调控一系列信号分子诱导血管生成拟态(VM)的形成。VM是一种缺氧驱动肿瘤细胞自身胞外基质重塑、不依赖内皮细胞的肿瘤血管形成方式,可在内皮源性肿瘤血管被抑制时依然为肿瘤供氧,故成为胶质瘤高侵袭性表型和治疗抗性的重要原因之一。因此,靶向血管拟态中ECM重塑关键因子及环节有望为胶质瘤治疗方案提供新思路。Extracellular matrix(ECM)is an important part of tumor microenvironment and participates in regulating the malignant phenotypes of various tumors. In glioma,the unique hypoxic microenvironment can stimulate cells and induce ECM remodeling,which provides space for tumor angiogenesis. Besides,hypoxia can induce the formation of vasculogenic mimicry(VM)by regulating a series of signaling molecules. VM is a special pattern of tumor angiogenesis via hypoxia-induced ECM remodeling in tumor cells and does not depend on endothelial cells,and it can supply oxygen to tumor even when endothelium-derived tumor vessels are inhibited,thus becoming one of the important causes of the high invasiveness and treatment resistance of gliomas. Therefore,identifying the key factors and links in ECM remodeling and VM formation are expected to provide new ideas for the treatment regimens for glioma.

关 键 词：胶质瘤 缺氧 肿瘤微环境 肿瘤血管发生 细胞外基质 

分 类 号：R739.[医药卫生—肿瘤]