Breast cancer-derived exosomes transmit lncRNA SNHG16 to induce CD73+γδ1 Treg cells
作者机构：Department of Breast SurgerySecond Affiliated HospitalZhejiang UniversityHangzhouZhejiang 310009China Key Laboratory of Tumour Microenvironment and Immune Therapy of Zhejiang ProvinceSecond Affiliated HospitalZhejiang UniversityHangzhouZhejiang 310009China Key Laboratory of Tumour Molecular Diagnosis and Individualized Medicine of Zhejiang ProvinceZhejiang Provincial People’s HospitalPeople’s Hospital of Hangzhou Medical CollegeHangzhouZhejiang 310014China Department of Thyroid and Breast SurgeryAffiliated Hospital of Shaoxing UniversityShaoxingZhejiang 312099China Department of Thyroid and Breast SurgeryZhejiang Provincial People’s HospitalPeople’s Hospital of Hangzhou Medical CollegeHangzhouZhejiang 310014China
出 版 物：《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗（英文）)
年 卷 期：2020年第5卷第1期
页 面：1953-1966页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：supported by the Zhejiang Medical and Health Science and Technology Plan Project(2019RC040 2017KY233) the Natural Science Foundation of China(81773065 and 81520108024) the Natural Science Foundation of Zhejiang Province(grant numbers LR19H160001,LY17C080001)
摘 要：γδT cells have been reported to exert immunosuppressive functions in multiple solid malignant diseases,but their immunosuppressive functional subpopulation in breast cancer(BC)is still ***,we collected 40 paired BC and normal tissue samples from Chinese patients for ***,we showed thatγδT1 cells comprise the majority of CD3+T cells in BC;next,we found that CD73+γδT1 cells were the predominant regulatory T-cell(Treg)population in BC,and that their prevalence in peripheral blood was also related to tumour *** addition,CD73+γδT1 cells exert an immunosuppressive effect via adenosine *** also found that BC could modulate CD73 expression onγδT cells in a non-contact *** microarray analysis and functional experiments indicated that breast tumour cell-derived exosomes(TDEs)could transmit lncRNA SNHG16,which upregulates CD73 expression,to Vδ1 T *** the mechanism,SNHG16 served as a ceRNA by sponging miR-16–5p,which led to the derepression of its target gene SMAD5 and resulted in potentiation of the TGF-β1/SMAD5 pathway to upregulate CD73 expression in Vδ1 T *** results showed that the BC-derived exosomal SNHG16/miR-16–5p/SMAD5-regulatory axis potentiates TGF-β1/SMAD5 pathway activation,thus inducing CD73 expression in Vδ1 T *** results first identify the significance of CD73+Vδ1 Tregs in BC,and therapy targeting this subpopulation or blocking TDEs might have potential for BC treatment in the future.
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