Chemoattractant receptors as pharmacological targets for elimination of glioma stem-like cells.
Chemoattractant receptors as pharmacological targets for elimination of glioma stem-like cells.
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DOI：
10.1016/j.intimp.2011.08.021
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发表时间：
2011-12
影响因子：
5.6
通讯作者：
Wang JM
中科院分区：
文献类型：
--
作者：
Yao XH;Liu Y;Chen K;Gong W;Liu MY;Bian XW;Wang JM
恶性肿瘤被认为是由一小群显示干细胞特性的细胞引发的，干细胞特性包括自我更新、多能分化、肿瘤组织的引发和对治疗的抗性的能力。癌症干细胞（CSC）也已在神经胶质瘤中被鉴定，其中它们被命名为神经胶质瘤干细胞样细胞（GSLC）或神经胶质瘤干细胞。在异种移植模型中，GSLCs增殖肿瘤并促进肿瘤进展。GSLCs的成瘤不仅依赖于其自主增殖，还依赖于与微环境成分的相互作用。其中G蛋白偶联趋化因子受体（G protein coupled chemoattractant receptor，GPCRs）及其激动剂因其介导白细胞浸润、血管生成、肿瘤侵袭和转移的功能而备受关注。趋化剂GPCR由肿瘤细胞和基质细胞广泛表达，并识别肿瘤微环境中存在的激动剂。已经发现这样的GPCR也由CSC（包括GSLC）表达。本文就胶质瘤细胞趋化因子GPCRs的功能、调控及信号转导等方面的研究进展作一综述，以期为进一步了解胶质瘤发生发展的机制和寻找新的抗胶质瘤治疗靶点提供参考。
Malignant tumors are thought to be initiated by a small population of cells that display stem cell properties, including the capacity of self-renewal, multipotent differentiation, initiation of tumor tissues and resistance to therapy. Cancer stem cells (CSCs) have also been identified in gliomas in which they are named as glioma stem-like cells (GSLCs), or glioma stem cells. In xenograft transplantation models, GSLCs propagate tumor and promote tumor progression. The tumorigenesis of GSLCs depends not only on their autonomous proliferation but also on interaction with microenvironment components. Among these components, G protein coupled chemoattractant receptors (GPCRs) and their agonists have attracted much attention for their capacity to mediate leukocyte infiltration, angiogenesis, tumor invasion and metastasis. Chemoattractant GPCRs are widely expressed by tumor cells and stromal cells and recognize agonists present in the tumor microenvironment. Such GPCRs have been found to be expressed also by CSCs including GSLCs. In this brief review, we will summarize the recent development in the studies of the function, regulation and signal transduction of chemoattractant GPCRs in GSLCs in hope to promote a better understanding of the mechanistic basis of the progression of gliomas and the identification of molecular targets for the novel anti-glioma therapy.
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影响因子：
11.2
作者：
Folkins C;Shaked Y;Man S;Tang T;Lee CR;Zhu Z;Hoffman RM;Kerbel RS
通讯作者：
Kerbel RS
影响因子：
11.2
作者：
Huang, Jian;Hu, Jinyue;Wang, Ji Ming
通讯作者：
Wang, Ji Ming
影响因子：
11.2
作者：
Biddle, Adrian;Liang, Xiao;Mackenzie, Ian C.
通讯作者：
Mackenzie, Ian C.
影响因子：
11.2
作者：
Collins, AT;Berry, PA;Maitland, NJ
通讯作者：
Maitland, NJ
DOI：
10.1073/pnas.0900244106
发表时间：
2009-03-10
影响因子：
11.1
作者：
Coffelt, Seth B.;Marini, Frank C.;Scandurro, Aline B.
通讯作者：
Scandurro, Aline B.