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Regulation of antitumor immunity by inflammation-induced epigenetic alterations

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Cellular & Molecular Immunology 2022年第1期19卷 59-66页

作者： Michael Karin Shabnam Shalapour Department of Pharmacology School of MedicineUniversity of California San DiegoLa JollaCAUSA Laboratory of Gene Regulation and Signal Transduction Department of PharmacologySchool of MedicineUniversity of California San DiegoLa JollaCAUSA Department of Cancer Biology University of Texas MD Anderson Cancer CenterHoustonTXUSA

Chronic inflammation promotes tumor development,progression,and metastatic dissemination and causes treatment *** accumulation of genetic alterations and loss of normal cellular regulatory processes are not only associated with cancer growth and progression but also result in the expression of tumor-specific and tumor-associated antigens that may activate antitumor *** antagonism between inflammation and immunity and the ability of cancer cells to avoid immune detection affect the course of cancer development and treatment *** inflammation,particularly acute inflammation,supports T-cell priming,activation,and infiltration into infected tissues,chronic inflammation is mostly ***,the main mechanisms that dictate the outcome of the inflammation-immunity interplay are not well *** data suggest that inflammation triggers epigenetic alterations in cancer cells and components of the tumor *** alterations can affect and modulate numerous aspects of cancer development,including tumor growth,the metabolic state,metastatic spread,immune escape,and immunosuppressive or immunosupportive leukocyte *** this review,we discuss the role of inflammation in initiating epigenetic alterations in immune cells,cancer-associated fibroblasts,and cancer cells and suggest how and when epigenetic interventions can be combined with immunotherapies to improve therapeutic outcomes.

关键词： Inflammation Epigenetics antitumor immunity Immunotherapy

Targeting the chromatin structural changes of antitumor immunity

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Journal of Pharmaceutical Analysis 2024年第4期14卷 460-482页

作者： Nian-nian Li Deng-xing Lun Ningning Gong Gang Meng Xin-ying Du He Wang Xiangxiang Bao Xin-yang Li Ji-wu Song Kewei Hu Lala Li Si-ying Li Wenbo Liu Wanping Zhu Yunlong Zhang Jikai Li Ting Yao Leming Mou Xiaoqing Han Furong Hao Yongcheng Hu Lin Liu Hongguang Zhu Yuyun Wu Bin Liu Weifang People's Hospital WeifangShandong261000China School of Life Sciences Nankai UniversityTianjin300071China Weifang Traditional Chinese Medicine Hospital WeifangShandong261000China Shaanxi Key Laboratory of Sericulture Ankang UniversityAnkangShaanxi725000China Guizhou Education University Guiyang550018China Guizhou Normal University Guiyang550025China School of Medical Imaging Weifang Medical UniversityWeifangShandong261053China Department of Bone and Soft Tissue Oncology Tianjin HospitalTianjin300299China Xinqiao Hospital of Army Military Medical University Chongqing400038China Teda Institute of Biological Sciences&Biotechnology Nankai UniversityTianjin300457China

Epigenomic imbalance drives abnormal transcriptional processes,promoting the onset and progression of *** defective gene regulation generally affects carcinogenesis and tumor suppression networks,tumor immunogenicity and immune cells involved in antitumor responses may also be affected by epigenomic changes,which may have significant implications for the development and application of epigenetic therapy,cancer immunotherapy,and their ***,we focus on the impact of epigenetic regulation on tumor immune cell function and the role of key abnormal epigenetic processes,DNA methylation,histone post-translational modification,and chromatin structure in tumor immunogenicity,and introduce these epigenetic research *** emphasize the value of small-molecule inhibitors of epigenetic modulators in enhancing antitumor immune responses and discuss the challenges of developing treatment plans that combine epigenetic therapy and immuno-therapy through the complex interaction between cancer epigenetics and cancer immunology.

关键词： antitumor immunity Chromatin structural Cancer epigenetics DNA methylation Histone modification Chemotherapy

CFTR is a negative regulator ofγδT cell IFN-γproduction and antitumor immunity

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Cellular & Molecular Immunology 2021年第8期18卷 1934-1944页

作者： Yuanyuan Duan Guangqiang Li Miaomiao Xu Xiaofei Qi Mingxia Deng Xuejia Lin Zhiwei Lei Yi Hu Zhenghu Jia Quanli Yang Guangchao Cao Zonghua Liu Qiong Wen Zhenhua Li Jie Tang Wei Kevin Zhang Pingbo Huang Limin Zheng Richard A.Flavell Jianlei Hao Zhinan Yin Zhuhai Precision Medical Center Zhuhai People’s Hospital(Zhuhai Hospital Affiliated with Jinan University)Jinan UniversityZhuhai519000GuangdongChina The Biomedical Translational Research Institute Faculty of Medical ScienceJinan UniversityGuangzhou510632GuangdongChina Department of Physiology School of Basic Medical SciencesSouthern Medical UniversityGuangzhou510515GuangdongChina The First Affiliated Hospital Jinan UniversityGuangzhou510632China School of Pharmaceutical Sciences South-Central University for NationalitiesWuhan430074HubeiChina Division of Life Science Hong Kong University of Science and Technology(HKUST)Hong KongChina State Key Laboratory of Oncology in Southern China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou510060China Department of Immunobiology School of MedicineYale UniversityNew HavenCT06520USA

CFTR,a chloride channel and ion channel regulator studied mostly in epithelial cells,has been reported to participate in immune regulation and likely affect the risk of cancer ***,little is known about the effects of CFTR on the differentiation and function ofγδT *** this study,we observed that CFTR was functionally expressed on the cell surface ofγδT *** deletion and pharmacological inhibition of CFTR both increased IFN-γrelease by peripheralγδT cells and potentiated the cytolytic activity of these cells against tumor cells both in vitro and in ***,the molecular mechanisms underlying the regulation ofγδT cell IFN-γproduction by CFTR were either TCR dependent or related to Ca^(2+)*** was recruited to TCR immunological synapses and attenuated Lck-P38 MAPK-c-Jun *** addition,CFTR was found to modulate TCR-induced Ca^(2+)influx and membrane potential(Vm)-induced Ca^(2+)influx and subsequently regulate the calcineurin-NFATc1 signaling pathway inγδT ***,CFTR serves as a negative regulator of IFN-γproduction inγδT cells and the function of these cells in antitumor *** investigation suggests that modification of the CFTR activity ofγδT cells may be a potential immunotherapeutic strategy for cancer.

关键词： CFTR γδT cells TCR Membrane potential antitumor immunity

LncRNA MEG3 promotes chemosensitivity of osteosarcoma by regulating antitumor immunity via miR-21-5p/p53 pathway and autophagy

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Genes & Diseases 2023年第2期10卷 531-541页

作者： Xin Huang Weiyue Zhang Feifei Pu Zhicai Zhang Department of Orthopaedics Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Department of Endocrinology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China

This study aimed to investigate the role of long non-coding RNA maternally expressed gene 3(lncRNA MEG3)in chemosensitivity of osteosarcoma(OS),and to reveal the possible underlying *** this study,we found that the expression of lncRNA MEG3 was significantly lower in OS tissues and cell ***,lncRNA MEG3 overexpression enhanced chemosensitivity of OS by inhibiting cell proliferation,migration,autophagy,and promoting antitumor *** MEG3 functioned as miR-21-5 sponge to regulate p53 expression in ***,lncRNA MEG3 promoted OS chemosensitivity by regulating antitumor immunity via miR-21-5p/p53 pathway and ***,this study provided the evidence that lncRNA MEG3 might be a promising therapeutic target for OS chemoresistance.

关键词： antitumor immunity Autophagy Chemosensitivity LncRNAMEG3 Osteosarcoma

Demethylzeylasteral induces PD-L1 ubiquitin-proteasome degradation and promotes antitumor immunity via targeting USP22

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Acta Pharmaceutica Sinica B 2024年第10期14卷 4312-4328页

作者： Yanyan Zhang Yun Huang Dianping Yu Mengting Xu Hongmei Hu Qing Zhang Minchen Cai Xiangxin Geng Hongwei Zhang Jianhua Xia Mengmeng Guo Dong Lu Hanchi Xu Linyang Li Xing Zhang Qun Wang Sanhong Liu Weidong Zhang Shanghai Frontiers Science Center of TCM Chemical Biology Institute of Interdisciplinary Integrative Medicine ResearchShanghai University of Traditional Chinese MedicineShanghai 201203China Department of Phytochemistry School of PharmacySecond Military Medical UniversityShanghai 200433China Institute of Medicinal Plant Development Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100193China The Research Center for Traditional Chinese Medicine Shanghai Institute of Infectious Diseases and BiosafetyInstitute of Interdisciplinary Integrative Medicine ResearchShanghai University of Traditional Chinese MedicineShanghai 201203China

Programmed cell death ligand-1(PD-L1)is a T cell inhibitory immune checkpoint molecule that interacts with programmed cell death-1(PD-1)to promote immune escape of tumor *** with antibody therapies,small molecule drugs show better prospects due to their advantages such as higher bioavailability,better tissue penetration,and reduced risk of ***,we found that the small molecule demethylzeylasteral(Dem)can significantly downregulate the expression of PD-L1 in colorectal cancer cells and enhance the killing effect of T cells on tumor ***,Dem binds to the deubiquitinating enzyme USP22 and promotes its degradation,resulting in increased ubiquitination and degradation of PD-L1 through the proteasome *** addition,Dem increased the activity of cytotoxic T cells and reduced the number of myeloid-derived suppressor cells(MDSCs)and regulatory T cells(Tregs)in tumor-infiltrating lymphocytes(TILs),thereby activating the tumor immune microenvironment and inhibiting the growth of subcutaneous MC38 tumors in C57BL/6 ***,we also found that the combination of Dem and CTLA4 antibodies can further improve the efficacy of antitumor *** study reveals the mechanism by which Dem promotes PD-L1 degradation and suggests that the combination of Dem and CTLA4 antibodies may improve the efficacy of immunotherapy.

关键词： Demethylzeylasteral PD-L1 USP22 Deubiquitination Tumor-infiltrating lymphocytes Colorectal cancer Immune checkpoint blockade antitumor immunity

TGR5 deficiency activates antitumor immunity in non-small cell lung cancer via restraining M2 macrophage polarization

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Acta Pharmaceutica Sinica B 2022年第2期12卷 787-800页

作者： Lifang Zhao Hongyan Zhang Xueqing Liu Shan Xue Dongfang Chen Jing Zou Handong Jiang Department of Respiratory and Critical Care Medicine Ren Ji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200127China

The bile acid-responsive G-protein-coupled receptor TGR5 is expressed in monocytes and macrophages,and plays a critical role in regulating inflammatory *** previous work has shown its role in promoting the progression of non-small cell lung cancer(NSCLC),yet the mechanism remains ***,using Tgr5-knockout mice,we show that TGR5 is required for M2 polarization of tumorassociated macrophages(TAMs)and suppresses antitumor immunity in NSCLC via involving TAMsmediated CD8+T cell ***,we demonstrate that TGR5 promotes TAMs into protumorigenic M2-like phenotypes via activating c AMP-STAT3/STAT6 *** of c AMP production restores M2-like phenotypes in TGR5-deficient *** NSCLC tissues from human patients,the expression of TGR5 is associated with the infiltration of *** co-expression of TGR5 and high TAMs infiltration are associated with the prognosis and overall survival of NSCLC ***,this study provides molecular mechanisms for the protumor function of TGR5 in NSCLC,highlighting its potential as a target for TAMs-centric immunotherapy in NSCLC.

关键词： TGR5 Bile acids Tumor-associated macrophages(TAMs) Tumor microenvironment(TME) Non-small cell lung cancer(NSCLC) antitumor immunity Immunotherapy c AMP-STAT3/STAT6

Myc inhibition tips the immune balance to promote antitumor immunity

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Cellular & Molecular Immunology 2022年第9期19卷 1030-1041页

作者： Chao Yang Yun Liu Yudi Hu Liang Fang Zhe Huang Huanhuan Cui Jun Xie Yazhen Hong Wei Chen Nengming Xiao Qiyuan Li Wen-Hsien Liu Changchun Xiao State Key Laboratory of Cellular Stress Biology School of Life SciencesFaculty of Medicine and Life SciencesXiamen UniversityXiamen361102FujianChina Institute of Hematology School of MedicineXiamen UniversityXiamen361102FujianChina Shenzhen Key Laboratory of Gene Regulation and Systems Biology School of Life Sciences and Academy for Advanced Interdisciplinary StudiesSouthern University of Science and TechnologyShenzhen518005GuangdongChina Sanofi Institute for Biomedical Research Suzhou215123JiangsuChina Department of Immunology and Microbiology The Scripps Research InstituteLa JollaCA92037USA

Aberrant expression of Myc is one of the most common oncogenic events in human *** of Myc inhibitors are currently under development for treating Myc-driven *** addition to directly targeting tumor cells,Myc inhibition has been shown to modulate the tumor microenvironment to promote tumor ***,the effect of Myc inhibition on immune cells in the tumor microenvironment remains poorly ***,we show that the adaptive immune system plays a vital role in the antitumor effect of pharmacologic inhibition of *** genetic and pharmacologic approaches,we found that Myc inhibition enhanced CD8 T cell function by suppressing the homeostasis of regulatory T(Treg)cells and the differentiation of resting Treg(rTreg)cells to activated Treg(aTreg)cells in ***,we demonstrated that different Myc expression levels confer differential sensitivity of T cell subsets to pharmacologic inhibition of *** ablation of the Myc gene has been shown to suppress CD8 T cell function,Treg cells,which express much less Myc protein than CD8 T cells,are more sensitive to Myc *** differential sensitivity of CD8 T and Treg cells to Myc inhibitors resulted in enhanced CD8 T cell function upon Myc *** findings revealed that Myc inhibitors can induce an antitumor immune response during tumor progression.

关键词： Myc inhibition Regulatory T cells Differential sensitivity antitumor immunity Cancer immunotherapy

OTUD5 promotes innate antiviral and antitumor immunity through deubiquitinating and stabilizing STING

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Cellular & Molecular Immunology 2021年第8期18卷 1945-1955页

作者： Yunyun Guo Fei Jiang Lingli Kong Haifeng Wu Honghai Zhang Xiaorong Chen Jian Zhao Baoshan Cai Yanqi Li Chunhong Ma Fan Yi Lei Zhang Bingyu Liu Yi Zheng Lingqiang Zhang Chengjiang Gao Key Laboratory of Infection and immunity of Shandong Province&Department of Immunology School of Biomedical SciencesShandong University250012JinanShandongPeople’s Republic of China Department of Pharmacology School of Biomedical SciencesShandong University250012JinanShandongPeople’s Republic of China State Key Laboratory of Proteomics Beijing Proteome Research CenterNational Center for Protein Sciences(Beijing)Beijing Institute of Lifeomics100850BeijingPeople’s Republic of China

Stimulator of interferon genes(STING)is an adaptor protein that is critical for effective innate antiviral and antitumor *** activity of STING is heavily regulated by protein ubiquitination,which is fine-tuned by both E3 ubiquitin ligases and ***,we report that the deubiquitinase OTUD5 interacts with STING,cleaves its K48-linked polyubiquitin chains,and promotes its ***,knockout of OTUD5 resulted in faster turnover of STING and subsequently impaired type I IFN signaling following cytosolic DNA *** importantly,Lyz2-Cre Otud5^(fl/Y) mice and CD11-Cre Otud5^(fl/Y) mice showed more susceptibility to herpes simplex virus type 1(HSV-1)infection and faster development of melanomas than their corresponding control littermates,indicating that OTUD5 is indispensable for STING-mediated antiviral and antitumor *** data suggest that OTUD5 is a novel checkpoint in the cGAS-STING cytosolic DNA sensing pathway.

关键词： Antiviral innate immunity antitumor immunity STING deubiquitination OTUD5

CD4^(+) T cell-released exosomes inhibit CD8^(+) cytotoxic T-lymphocyte responses and antitumor immunity

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Cellular & Molecular Immunology 2011年第1期8卷 23-30页

作者： Haifeng Zhang Yufeng Xie Wei Li Rajni Chibbar Sidong Xiong Jim Xiang Research Unit Health Research DivisionSaskatchewan Cancer AgencyDepartment of Oncology and ImmunologyUniversity of SaskatchewanSaskatoonSask.Canada Research Unit Health Research DivisionSaskatchewan Cancer AgencyDepartment of PathologyUniversity of SaskatchewanSaskatoonSask.Canada Institute of Biology and Medical Sciences Soochow UniversitySuzhouChina

T cells secrete bioactive exosomes(EXO),but the potential immunoregulatory effect of T-cell EXO is largely *** this study,we generated activated ovalbumin(OVA)-specific CD4^(+) T cells in vitro via coculture of OVA-pulsed dendritic cells(DC_(OVA))with naive CD4^(+) T cells derived from OVA-specific T-cell receptor(TCR)transgenic OTII ***4^(+) T-cell EXO were then purified from the CD4^(+) T-cell culture supernatants by differential ***4^(+) T-cell EXO exhibited the‘saucer’shape that is characteristic of EXO with a diameter between 50 and 100 nm,as assessed by electron microscopy,and contained the EXO-associated proteins LAMP-1,TCR and lymphocyte function associated antigen-1(LFA-1),as determined by western *** cytometric analysis showed that CD4^(+) T-cell EXO expressed CD4^(+) T-cell markers(CD4,TCR,LFA-1,CD25 and Fas ligand),but to a lesser extent than CD4^(+) T *** demonstrated that DC_(OVA) took up CD4^(+) T-cell EXO via peptide/major histocompatibility complex(pMHC)II/TCR and CD54/LFA-1 ***-specific CD4^(+) T-cell EXO from OTII mice,but not ConA-stimulated polyclonal CD4^(+) T-cell EXO from wild-type C57BL/6 mice inhibited DC_(OVA)-stimulated in vitro CD4^(+) T-cell proliferation and in vivo CD81 cytotoxic T lymphocyte(CTL)responses and antitumor immunity against OVA-expressing B16 melanoma BL6-10OVA *** addition,EXO derived from a T-cell hybridoma cell line,MF72.2D9,expressing an OVA-specific CD4^(+) TCR,had a similar inhibitory effect as OTII CD4^(+) T-cell EXO on CTL-mediated antitumor *** together,our data indicate that antigen-specific T-cell EXO may serve as a new type of immunosuppressive reagent for use in transplant rejection and treatment of autoimmune diseases.

关键词： antitumor immunity CTL T-cell exosome