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TREML2通过抑制NF-κB/CXCL10信号通路增强急性髓系白血病细胞对化疗的敏感性。

TREML2 enhances sensitivity of acute myeloid leukemia cells to chemotherapy by inhibiting the NF-κB/CXCL10 pathway.

作者信息

Zhang Xin, Yan Shuheng, Zhang Xuehong, Huang Dan, Zhou Jiayin, Song Xiaoting, Hao Yuchao, Wang Xijia, Yan Jinsong

机构信息

Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, Liaoning Key Laboratory of Hematopoietic Stem Cell Transplantation and Translational Medicine, Blood Stem Cell Transplantation Institute, Dalian Key Laboratory of Hematology, Diamond Bay Institute of Hematology, the Second Hospital of Dalian Medical University, Dalian, China.

University of California, Davis, College of Biological Science, 1 Shields Ave, Davis, CA 95616, United States.

出版信息

Blood Sci. 2025 Mar 18;7(2):e00223. doi: 10.1097/BS9.0000000000000223. eCollection 2025 Jun.

DOI:10.1097/BS9.0000000000000223
PMID:40109578
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11922426/
Abstract

The triggering receptors expressed on myeloid cells (TREMs) family of cell surface receptors are mainly expressed by myeloid cells. The expression profile of TREM-like 2 (TREML2), a TREM family member, in patients with acute myeloid leukemia (AML) is unknown. In this study, we aimed to elucidate the role of TREML2 in the development of AML. We analyzed the TREML2 expression profile in patients with AML. TREML2 was expressed at lower levels in patients with AML than in healthy individuals. The partial remission (PR) + no remission (NR) group showed lower TREML2 expression levels and a poorer chemotherapy response than that observed in the complete remission group. Overall survival was significantly shorter in the group with low TREML2 expression levels than in the group with high TREML2 expression levels. TREML2 inhibited the proliferation of AML cells and enhanced the sensitivity of AML cells to doxorubicin. Mechanistically, TREML2 reduced C-X-C motif chemokine ligand 10 expression levels by inhibiting the nuclear factor kappa B pathway. Taken together, we demonstrate that TREML2 has diagnostic value as a potential indicator of AML and that upregulation of TREML2 may be a new strategy to overcome doxorubicin resistance for AML treatment.

摘要

髓系细胞表达的触发受体（TREMs）家族的细胞表面受体主要由髓系细胞表达。TREM家族成员之一的类TREM 2（TREML2）在急性髓系白血病（AML）患者中的表达情况尚不清楚。在本研究中，我们旨在阐明TREML2在AML发生发展中的作用。我们分析了AML患者的TREML2表达情况。与健康个体相比，AML患者中TREML2的表达水平较低。部分缓解（PR）+未缓解（NR）组的TREML2表达水平低于完全缓解组，化疗反应也较差。TREML2表达水平低的组的总生存期明显短于TREML2表达水平高的组。TREML2抑制AML细胞的增殖，并增强AML细胞对阿霉素的敏感性。机制上，TREML2通过抑制核因子κB途径降低C-X-C基序趋化因子配体10的表达水平。综上所述，我们证明TREML2作为AML的潜在指标具有诊断价值，上调TREML2可能是克服AML治疗中阿霉素耐药的一种新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/5086635b77b5/bs9-7-e00223-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/31b8c334c5d6/bs9-7-e00223-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/7fb476068295/bs9-7-e00223-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/70cce49444a3/bs9-7-e00223-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/27e945245f6b/bs9-7-e00223-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/87d83210a18c/bs9-7-e00223-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/5d8217fa6a09/bs9-7-e00223-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/5086635b77b5/bs9-7-e00223-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/31b8c334c5d6/bs9-7-e00223-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/7fb476068295/bs9-7-e00223-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/70cce49444a3/bs9-7-e00223-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/27e945245f6b/bs9-7-e00223-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/87d83210a18c/bs9-7-e00223-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/5d8217fa6a09/bs9-7-e00223-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bd/11922426/5086635b77b5/bs9-7-e00223-g007.jpg

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