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GATA1-mediated Notch signaling augment antitumor immunity of CD11b+CD27-natural killer cells maturation via BCL9/β-catenin signal

文献类型：期刊论文

作者Yang, Fan10,11; Li, Anqi10,11; Zhu, Yuanyuan10,11; Zhou, Yan8,9; Tian, Enming10,11; Yang, Mengxuan6,7; Zhou, Qingtong8,9; Yang, Dehua8,9; Wang, Ming-Wei8,9; Feng, Mei5
刊名CELL REPORTS
出版日期2025-05-27
卷号44期号:5页码:23
ISSN号2211-1247
DOI10.1016/j.celrep.2025.115708
通讯作者Wang, Ming-Wei(mwwang@simm.ac.cn) ; Feng, Mei(fm_fudan@163.com) ; Zhu, Di(zhudi@fudan.edu.cn)
英文摘要The maturation process of natural killer (NK) cells is integral to their antitumor immune response. Despite the diverse effector properties exhibited during differentiation, targeting the fate of NK cells for immunotherapy remains challenging. Here, we demonstrate that deficiency of B cell lymphoma 9 (BCL9) induces transient expression of GATA1 in CD11b+ CD27-NK cells upon activation of Notch and interleukin-18 receptor 1 (IL-18R1) signaling, which are crucial for their maturation and antitumor activity. Conversely, blocking Notch signaling impairs NK cell development and antitumor function. NK-specific Bcl9-deficiency enhances B16F10 tumor killing in vivo. Our findings underscore the intricate network interactions among transcription factors, signal transduction pathways in development, and cytokines modulated by BCL9 deficiency. Targeting BCL9 emerges as a promising strategy for melanoma therapy, bolstering NK cell maturation and cytotoxicity, and overcoming challenges in NK cell-based immunotherapies.
WOS关键词NK-CELL ; B-CELL ; BETA-CATENIN ; T-CELL ; WNT ; EXPRESSION ; INNATE ; STABILIZATION ; REQUIREMENT ; INVOLVEMENT
资助项目Shanghai Sailing Program[23YF1407600] ; China Postdoctoral Science Foundation[2022TQ0079] ; National Natural Science Foundation of China[82273952] ; National Natural Science Foundation of China[81872895] ; National Natural Science Foundation of China[82073881] ; National Natural Science Foundation of China[82303177] ; Innovative Drug and Evaluation Innovation Team for Tumor Immunotherapy of Jinan Science and Technology Bureau[2020GXRC041] ; Science and Technology Commission of Shanghai[18ZR1403900] ; Science and Technology Commission of Shanghai[20430713600]
WOS研究方向Cell Biology
语种英语
WOS记录号WOS:001513812600001
出版者CELL PRESS
源URL[http://119.78.100.183/handle/2S10ELR8/318624]  
专题中国科学院上海药物研究所
通讯作者Wang, Ming-Wei; Feng, Mei; Zhu, Di
作者单位1.Guilin Med Univ, Affiliated Hosp 2, Dept Oncol, Guilin 541199, Peoples R China
2.Guilin Med Univ, Affiliated Hosp 2, Key Lab Tumor Immunol & Microenvironm Regulat, Guilin 541199, Peoples R China
3.Fudan Univ, Shanghai Canc Ctr, Shanghai 200032, Peoples R China
4.Shandong Acad Pharmaceut Sci, Jinan 250101, Peoples R China
5.Fudan Univ, Sch Basic Med Sci, Dept Pharmacol, Shanghai 201100, Peoples R China
6.Fudan Univ, Sch Pharm, Shanghai 201203, Peoples R China
7.Fudan Univ, Minhang Hosp, Dept Pharmacol, Shanghai 201203, Peoples R China
8.Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China
9.Chinese Acad Sci, Shanghai Inst Mat Med, Natl Ctr Drug Screening, Shanghai 201203, Peoples R China
10.Fudan Univ, Shanghai Engn Res Ctr Immune Therapy, Sch Pharm, Shanghai 201203, Peoples R China
推荐引用方式
GB/T 7714		 Yang, Fan,Li, Anqi,Zhu, Yuanyuan,et al. GATA1-mediated Notch signaling augment antitumor immunity of CD11b+CD27-natural killer cells maturation via BCL9/β-catenin signal[J]. CELL REPORTS,2025,44(5):23.
APA Yang, Fan.,Li, Anqi.,Zhu, Yuanyuan.,Zhou, Yan.,Tian, Enming.,...&Zhu, Di.(2025).GATA1-mediated Notch signaling augment antitumor immunity of CD11b+CD27-natural killer cells maturation via BCL9/β-catenin signal.CELL REPORTS,44(5),23.
MLA Yang, Fan,et al."GATA1-mediated Notch signaling augment antitumor immunity of CD11b+CD27-natural killer cells maturation via BCL9/β-catenin signal".CELL REPORTS 44.5(2025):23.

入库方式： OAI收割

来源：上海药物研究所

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