CD11c公司
癌症干细胞
生物
癌症研究
胶质瘤
干细胞
人口
肿瘤微环境
肿瘤进展
免疫系统
癌细胞
移植
骨髓
免疫学
癌症
细胞生物学
医学
内科学
表型
基因
生物化学
环境卫生
遗传学
作者
Yasuhiro Kokubu,Kouichi Tabu,Nozomi Muramatsu,Wenqian Wang,Yoshitaka Murota,Ikuo Nobuhisa,Masahisa Jinushi,Tetsuya Taga
摘要
Cancer stem cells (CSCs) are maintained under special microenvironment called niche, and elucidation and targeting of the CSC niche will be a feasible strategy for cancer eradication. Tumor-associated macrophages (TAMs) are known to be involved in cancer progression and thus can be a component of CSC niche. Although TAMs are known to play multiple roles in tumor progression, involvement of CSCs in TAM development fully remains to be elucidated. Using rat C6 glioma side population (SP) cells as a model of glioma CSCs, we here show that CSCs induce the TAM development by promoting survival and differentiation of bone marrow-derived monocytes. CSC-induced macrophages can be separated into two distinct subsets of cells, CD11c(low) and CD11c(high) cells. Interestingly, only the CD11c(high) subset of cells have protumoral activity, as shown by intracranial transplantation into immune-deficient mice together with CSCs. These CD11c(high) macrophages were observed in the tumor formed by co-transplantation with CSCs. Furthermore, CSCs produced GM-CSF and anti-GM-CSF antibody inhibited CSC-induced TAM development. In conclusion, CSCs have the ability to self-create their own niche involving TAMs through CSC-derived GM-CSF, which can thus be a therapeutic target in view of CSC niche disruption.
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