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作 者:Teng Ma Yu Tang Taolin Wang Yang Yang Yige Zhang Ruihuan Wang Yongxin Zhang Yi Li Mingbo Wu Miao Tang Xueli Hu Chaoyu Zou Yuan Ren Huan Liu Qianhua Zhang Heyue Li Min Wu Jing Li Xikun Zhou
机构地区:[1]Department of Biotherapy,Cancer Center and State Key Laboratory of Biotherapy,West China Hospital,Sichuan University,610041 Chengdu,China [2]Department of Breast Surgery,Sichuan Provincial People’s Hospital,University of Electronic Science and Technology of China,610072 Chengdu,China [3]State Key Laboratory of Oral Diseases,National Clinical Research Center for Oral Diseases,Research Unit of Oral Carcinogenesis and Management,Chinese Academy of Medical Sciences,West China Hospital of Stomatology,Sichuan University,Chengdu,China [4]Drug Discovery Center,Wenzhou Institute,University of Chinese Academy of Sciences,325001 Wenzhou,China
出 处:《Signal Transduction and Targeted Therapy》2023年第9期4305-4319,共15页信号转导与靶向治疗(英文)
基 金:This work was supported by the National Natural Science Foundation of China(No.81922042,82172285,82241049,82072999 and 82273320);the 1·3·5 project of excellent development of discipline of West China Hospital of Sichuan University(No.ZYYC21001);the Innovation Research Project of Sichuan University(No.2022SCUH0029);the CAMS Innovation Fund for Medical Sciences(CIFMS,2019-I2M-5-004).
摘 要:Breast cancer can metastasize to various organs,including the lungs.The immune microenvironment of the organs to be metastasized plays a crucial role in the metastasis of breast cancer.Infection with pathogens such as viruses and bacteria can alter the immune status of the lung.However,the effect of chronic inflammation caused by bacteria on the formation of a premetastatic niche within the lung is unclear,and the contribution of specific immune mediators to tumor metastasis also remains largely undetermined.Here,we used a mouse model revealing that chronic pulmonary bacterial infection augmented breast cancer lung metastasis by recruiting a distinct subtype of tumor-infiltrating MHCII^(hi) neutrophils into the lung,which exhibit cancer-promoting properties.Functionally,MHCII^(hi) neutrophils enhanced the lung metastasis of breast cancer in a cell-intrinsic manner.Furthermore,we identified CCL2 from lung tissues as an important environmental signal to recruit and maintain MHCII^(hi) neutrophils.Our findings clearly link bacterial-immune crosstalk to breast cancer lung metastasis and define MHCII^(hi) neutrophils as the principal mediator between chronic infection and tumor metastasis.
关 键 词:METASTASIS LUNG BREAST
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