M2-like tumor-associated macrophages drive vasculogenic mimicry through amplification of IL-6 expression in glioma cells
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- 英文论文题名：M2-like tumor-associated macrophages drive vasculogenic mimicry through amplification of IL-6 expression in glioma cells
- 论文作者：Zhang Lin ; Xu Yangyang ; Sun Jintang ; Chen Weiliang ; Zhao Lei ; Ma Chao ; Wang Qingjie ; Sun Jia ; Huang Bin ; Zhang Yun ; Li Xingang ; Qu Xun
- 英文论文作者：Zhang Lin ; Xu Yangyang ; Sun Jintang ; Chen Weiliang ; Zhao Lei ; Ma Chao ; Wang Qingjie ; Sun Jia ; Huang Bin ; Zhang Yun ; Li Xingang ; Qu Xun ; Institute of Basic Medical Sciences ; Qilu Hospital of Shandong University ; Key Laboratory of Cardiovascular Remodeling and Function Research ; Qilu Hospital ; School of Medicine ; Shandong University ; Department of Neurosurgery ; Qilu Hospital of Shandong University and Brain Science Research Institute ; Shandong University
- 年：2016
- 作者机构：Institute of Basic Medical Sciences,Qilu Hospital of Shandong University;Key Laboratory of Cardiovascular Remodeling and Function Research,Qilu Hospital,School of Medicine,Shandong University;Department of Neurosurgery,Qilu Hospital of Shandong University and Brain Science Research Institute,Shandong University;
- 英文论文关键词：macrophages ; glioma ; vasculogenic mimicry ; IL-6 ; PKC
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R739.41
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1011k
- 原文格式：D
- 会议级别：全国
摘要
The discovery of vasculogenic mimicry(VM) has offered a new horizon for understanding tumor angiogenesis, but the molecular 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. CD163 and VM were examined by immunohistochemistry. Tubule formation assays were used to estimate the VM of glioma cells that had received different treatments. qRT-PCR and Western blotting were used to estimate the protein level of VM markers. IL6 Secreted by glioma cells were measured by Cytokine Array and ELISA.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 regulate 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.
The discovery of vasculogenic mimicry(VM) has offered a new horizon for understanding tumor angiogenesis, but the molecular 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. CD163 and VM were examined by immunohistochemistry. Tubule formation assays were used to estimate the VM of glioma cells that had received different treatments. qRT-PCR and Western blotting were used to estimate the protein level of VM markers. IL6 Secreted by glioma cells were measured by Cytokine Array and ELISA.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 regulate 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.
The discovery of vasculogenic mimicry(VM) has offered a new horizon for understanding tumor angiogenesis, but the molecular 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. CD163 and VM were examined by immunohistochemistry. Tubule formation assays were used to estimate the VM of glioma cells that had received different treatments. qRT-PCR and Western blotting were used to estimate the protein level of VM markers. IL6 Secreted by glioma cells were measured by Cytokine Array and ELISA.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 regulate 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.
引文