Oncotarget

Research Papers:

IL-10 secreted by M2 macrophage promoted tumorigenesis through interaction with JAK2 in glioma

Ling Qi, Hongquan Yu, Yu Zhang, Donghai Zhao, Peng Lv, Yue Zhong and Ye Xu _

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2016; 7:71673-71685. https://doi.org/10.18632/oncotarget.12317

Metrics: PDF 1154 views  |   HTML 2170 views  |   ?  


Abstract

Ling Qi1, Hongquan Yu2, Yu Zhang2, Donghai Zhao1, Peng Lv1, Yue Zhong3, Ye Xu4

1The Department of Pathology, Jilin Medical University, Jilin 132013, PR China

2The Department of Neurosurgery, First Affiliated Hospital of Jilin University, Jilin 130021, PR China

3The Department of Science and Technology, Jilin Medical University, Jilin 132013, PR China

4The Medical Research Laboratory, Jilin Medical University, Jilin 132013, PR China

Correspondence to:

Yue Zhong, email: yuezhong_DST@126.com

Ye Xu, email: xuye_mpc@126.com

Keywords: glioma, M2 macrophage, proliferation, IL-10, JAK2/STAT3

Received: July 25, 2016     Accepted: September 22, 2016     Published: September 28, 2016

ABSTRACT

M2 tumor-associated macrophage has been found to play a supportive role in the progression of glioma. The underlying mechanism, nevertheless, has been largely unknown. In our study, to investigate how M2 macrophage played role in glioma, firstly we’ve analyzed the clinicopathological significance of M2 macrophage existence on clinical tissues of glioma using detection of CD163 expression with immunohistochemistry. Then, we’ve artificially induced M2 macrophage from human monocyte cell line THP-1, followed by co-culture with glioma cell lines in vitro. It was found that M2 macrophage was shown to be markedly distributed in glioma relative to paired normal control; and high prevalence of M2 macrophage was significantly associated with poorer overall survival and tumor progression. Moreover, M2 macrophage was found to be able to promote the growth in vitro and tumorigenesis in vivo in xenografted mice model. Mechanistically, it is IL-10 from M2 macrophage that was shown to promote proliferation, dependent on activation of JAK2/STAT3 pathway. Further, IL-10 was found to be able to interact with JAK2 in glioma cells. Taking together, we for the first time found that IL-10 from M2 macrophage promoted proliferation of glioma through interaction with JAK2; thereby activating the JAK2/STAT3 pathway, indicative of IL-10 could be used as a therapeutic target in the curing of glioma.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 12317