标题：M2-like tumor-associated macrophages drive vasculogenic mimicry through amplification of IL-6 expression in glioma cells
作者：Zhang, Lin; Xu, Yangyang; Sun, Jintang; Chen, Weiliang; Zhao, Lei; Ma, Chao; Wang, Qingjie; Sun, Jia; Huang, Bin; Zhang, Yun; Li, 更多 作者机构：[Zhang, Lin; Sun, Jintang; Zhao, Lei; Ma, Chao; Wang, Qingjie; Sun, Jia; Qu, Xun] Shandong Univ, Qilu Hosp, Inst Basic Med Sci, Jinan, Peoples R China 更多
通讯作者：Qu, X;Li, XG;Li, XG;Qu, X
通讯作者地址：[Qu, X]Shandong Univ, Qilu Hosp, Inst Basic Med Sci, Jinan, Peoples R China;[Li, XG]Shandong Univ, Qilu Hosp, Dept Neurosurg, Jinan, Peoples R China;[ 更多
关键词：Glioma; IL-6; Macrophages; PKC; Vasculogenic mimicry
摘要：Vasculogenic mimicry (VM) has offered a new horizon for understanding tumor angiogenesis, but the mechanisms of VM in glioma progression have not been studied explicitly until now. As a significant component of immune infiltration in tumor microenvironment, macrophages have been demonstrated to play an important role in tumor growth and angiogenesis. However, whether macrophages could play a potential key role in glioma VM is still poorly understood. Herein we reported that both VM and CD163(+) cells were associated with WHO grade and reduced patient survival, and VM channel counting was correlated to the number of infiltrated CD163+ cells in glioma specimens. In vitro studies of glioma cell lines implicated that M2-like macrophages (M2) promoted glioma VM. We found that conditional medium derived from M2 amplified IL-6 expression in glioma cells. Furthermore, our data indicated that IL-6 could promote glioma VM, as blocking IL-6 with neutralizing antibodies abrogated M2-mediated VM enhancement. In addition, the potent PKC inhibitor bisindolylmaleimide I could prevent M2-induced IL-6 upregulation and further inhibited glioma VM facilitation. Taken together, our results suggested that M2-like macrophages drove glioma VM through amplifying IL-6 secretion in glioma cells via PKC pathway.