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Hypoxia-induced TREM1 promotes mesenchymal-like states of glioma stem cells via alternatively activating tumor-associated macrophages

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资源类型：
Pubmed体系：
作者：
Dong Minhai[1] * ; Zhang Xiaolin[2] * ; Peng Peng[3] ; Chen Zirong[1] ; Zhang Yang[4] ; Wan Lijun[1] ; Xiang Wang[1] ; Liu Guohao[1] ; Guo Yang[1] ; Xiao Qungen[1] ; Wang Baofeng[1] ; Guo Dongsheng[1] ; Zhu Min[5,*3] ; Yu Xingjiang[4,*2] ; Wan Feng[3,*1] ;
单位： [1]Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China [2]Department of Neurosurgery, Guangdong Prov incial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 5 10080, China. [3]Department of Neurosurgery, X iangyang Central Hospital, A filiated Hospital to Hubei University of Arts and Science, Xiangyang, 44 13000, China [4]Department of Histology and Embryology, College of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [5]Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
出处：
DOI： 10.1016/j.canlet.2024.216801
ISSN：

关键词： Hypoxia Glioma stem cells Tumor-associated macrophages TREM1 Mesenchymal-like states

摘要：
The mesenchymal subtype of glioblastoma (GBM) cells characterized by aggressive invasion and therapeutic resistance is thought to be dependent on cell-intrinsic alteration and extrinsic cellular crosstalk. Tumor-associated macrophages (TAMs) are pivotal in tumor progression, chemo-resistance, angiogenesis, and stemness maintenance. However, the impact of TAMs on the shifts in glioma stem cells (GSCs) states remains largely uncovered. Herein, we showed that the triggering receptor expressed on myeloid cells-1 (TREM1) preferentially expressed by M2-like TAMs and induced GSCs into mesenchymal-like states by modulating the secretion of TGFβ2, which activated the TGFβR/SMAD2/3 signaling in GSCs. Furthermore, we demonstrated that TREM1 was transcriptionally regulated by HIF1a under the hypoxic environment and thus promoted an immunosuppressive type of TAMs via activating the TLR2/AKT/mTOR/c-MYC axis. Collectively, this study reveals that cellular communication between TAMs and GSCs through the TREM1-mediated TGFβ2/TGFβR axis is involved in the mesenchymal-like transitions of GSCs. Our study provides valuable insights into the regulatory mechanisms between the tumor immune microenvironment and the malignant characteristics of GBM, which can lead to potential novel strategies targeting TAMs for tumor control.Copyright © 2024. Published by Elsevier B.V.

基金：
This work was supported by the Program for the HUST Academic Frontier Y outh Team, the Huazhong University of Science and Technology Independent Innovation Research Fund Project (No. 2019kfyXJJS 187), National Natural Science F oundation of China (No.82072805, Xingjiang Yu; No.82072795, Feng Wan).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2023]版：
大类 | 1 区 医学
小类 | 2 区 肿瘤学
最新[2025]版：
大类 | 1 区 医学
小类 | 2 区 肿瘤学
第一作者：
第一作者单位： [1]Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
共同第一作者：
通讯作者：
通讯机构： [3]Department of Neurosurgery, X iangyang Central Hospital, A filiated Hospital to Hubei University of Arts and Science, Xiangyang, 44 13000, China [4]Department of Histology and Embryology, College of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [5]Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [*1]Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China [*2]Department of Histology and Embryology, College of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China [*3]Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
推荐引用方式(GB/T 7714)：
Dong Minhai,Zhang Xiaolin,Peng Peng,et al.Hypoxia-induced TREM1 promotes mesenchymal-like states of glioma stem cells via alternatively activating tumor-associated macrophages[J].Cancer Letters.2024,216801.doi:10.1016/j.canlet.2024.216801.
APA：
Dong Minhai,Zhang Xiaolin,Peng Peng,Chen Zirong,Zhang Yang...&Wan Feng.(2024).Hypoxia-induced TREM1 promotes mesenchymal-like states of glioma stem cells via alternatively activating tumor-associated macrophages.Cancer Letters,,
MLA：
Dong Minhai,et al."Hypoxia-induced TREM1 promotes mesenchymal-like states of glioma stem cells via alternatively activating tumor-associated macrophages".Cancer Letters .(2024):216801

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