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Pancreatic melatonin enhances anti-tumor immunity in pancreatic adenocarcinoma through regulating tumor-associated neutrophils infiltration and NETosis

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Acta Pharmaceutica Sinica B 2023年第4期13卷 1554-1567页

作者： Yau-tuen Chan Hor-yue Tan Yuanjun Lu Cheng Zhang Chien-shan Cheng Junyu Wu Ning Wang Yibin Feng School of Chinese Medicine the University of Hong KongHong KongChina Centre for Chinese Herbal Medicine Drug Development School of Chinese MedicineHong Kong Baptist UniversityHong KongChina Department of Traditional Chinese Medicine Shanghai Jiaotong UniversitySchool of Medicine Affiliated Ruijin HospitalShanghai 200025China

tumor microenvironment contributes to poor prognosis of pancreatic adenocarcinoma(PAAD)patients.Proper regulation could improve survival.Melatonin is an endogenous hormone that delivers multiple bioactivities.Here we showed that pancreatic melatonin level is associated with patients'survival.In PAAD mice models,melatonin supplementation suppressed tumor growth,while blockade of melatonin pathway exacerbated tumor progression.This anti-tumor effect was independent of cytotoxicity but associated with tumor-associated neutrophils(TANs),and TANs depletion reversed effects of melatonin.Melatonin induced TANs infiltration and activation,therefore induced cell apoptosis of PAAD cells.Cytokine arrays revealed that melatonin had minimal impact on neutrophils but induced secretion of Cxcl2 from tumor cells.Knockdown of Cxcl2 in tumor cells abolished neutrophil migration and activation.Melatonin-induced neutrophils presented an N1-like anti-tumor phenotype,with increased neutrophil extracellular traps(NETs)causing tumor cell apoptosis through cell-to-cell contact.Proteomics analysis revealed that this reactive oxygen species(ROS)-mediated inhibition was fueled by fatty acid oxidation(FAO)in neutrophils,while FAO inhibitor abolished the anti-tumor effect.Analysis of PAAD patient specimens revealed that CXCL2 expression was associated with neutrophil infiltration.CXCL2,or TANs,combined with NET marker,can better predict patients'prognosis.Collectively,we discovered an anti-tumor mechanism of melatonin through recruiting N1-neutrophils and beneficial NET formation.

关键词： Pancreatic adenocarcinoma Melatonin anti-tumor immunity tumor-associated neutrophils tumor microenvironment CXCL2 Neutrophil extracellular traps NETosis

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The crosstalk between ferroptosis and anti-tumor immunity in the tumor microenvironment:molecular mechanisms and therapeutic controversy

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Cancer Communications 2023年第10期43卷 1071-1096页

作者： Yichen Zheng Lingqi Sun Jiamin Guo Ji Ma Division of Abdominal tumor Multimodality Treatment Cancer CenterWest China HospitalSichuan UniversityChengduSichuanP.R.China Department of Neurology Air Force Hospital of the Western Theater of the Chinese People's Liberation ArmyChengduSichuanP.R.China

The advent of immunotherapy has significantly reshaped the landscape of cancer treatment,greatly enhancing therapeutic outcomes for multiple types of cancer.However,only a small subset of individuals respond to it,underscoring the urgent need for new methods to improve its response rate.Ferroptosis,a recently discovered form of programmed cell death,has emerged as a promising approach for anti-tumor therapy,with targeting ferroptosis to kill tumors seen as a potentially effective strategy.Numerous studies suggest that inducing ferroptosis can synergistically enhance the effects of immunotherapy,paving the way for a promising combined treatment method in the future.Nevertheless,recent research has raised concerns about the potential negative impacts on anti-tumor immunity as a consequence of inducing ferroptosis,leading to conflicting views within the scientific community about the interplay between ferroptosis and anti-tumor immunity,thereby underscoring the necessity of a comprehensive review of the existing literature on this relationship.Previous reviews on ferroptosis have touched on related content,many focusing primarily on the promoting role of ferroptosis on anti-tumor immunity while overlooking recent evidence on the inhibitory effects of ferroptosis on immunity.Others have concentrated solely on discussing related content either from the perspective of cancer cells and ferroptosis or from immune cells and ferroptosis.Given that both cancer cells and immune cells exist in the tumor microenvironment,a one-sided discussion cannot comprehensively summarize this topic.Therefore,from the perspectives of both tumor cells and tumor-infiltrating immune cells,we systematically summarize the current conflicting views on the interplay between ferroptosis and anti-tumor immunity,intending to provide potential explanations and identify the work needed to establish a translational basis for combined ferroptosis-targeted therapy and immunotherapy in treating tumors.

关键词： anti-tumor immunity ferroptosis ferroptosis-targeted therapy immunogenic cell death immunotherapy tumor microenvironment

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Immunomodulatory Function of Pien Tze Huang in T Cell-Mediated anti-tumor Activity against B16-F10,MC38 and Hep1-6 tumor Models

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Chinese Journal of Integrative Medicine 2024年第4期30卷 348-358页

作者： FU Yu-bing LIU Chen-feng WANG Jin-jia JI Xiao-lin TANG Rong-han LIAO Kun-yu CHEN Ling-yue HONG Ya-zhen FAN Bin-bin WANG Shi-cong LIU Wen-Hsien State Key Laboratory of Cellular Stress Biology School of Life SciencesFaculty of Medicine and Life ScienceXiamen UniversityXiamenFujian Province(361102)China Fujian Pien Tze Huang Enterprise Key Laboratory of Natural Medicine Research and Development ZhangzhouFujian Province(363000)China

Objective To investigate the anti-tumor effects of Pien Tze Huang(PZH)in mouse models of B16–F10 melanoma,MC38 colorectal cancer,Hep1-6 hepatocellular carcinoma and chemically induced hepatocellular carcinoma model.Methods Various tumor models,including B16–F10,MC38 and Hep1-6 tumor hypodermic inoculation models,B16–F10 and Hep1-6 pulmonary metastasis models,Hep1-6 orthotopic implantation model,and chemically induced hepatocellular carcinoma model,were utilized to evaluate the anti-tumor function of PZH.tumor growth was assessed by measuring tumor size and weight of solid tumors isolated from C57BL/6 mice.For cell proliferation and death of tumor cells in vitro,as well as T cell activation markers,cytokine production and immune checkpoints analysis,single-cell suspensions were prepared from mouse spleen,lymph nodes,and tumors after PZH treatment.Results PZH demonstrated significant therapeutic efficacy in inhibiting tumor growth(Ptumor size in subcutaneous MC38 colon adenocarcinoma and B16–F10 melanoma models,and decreased pulmonary metastasis of B16–F10 melanoma and Hep1-6 hepatoma(Ptumor cells(P>0.05).Nevertheless,PZH exhibited a remarkable ability to enhance T cell activation and the production of interferon gamma,tumor necrosis factor alpha,and interleukin 2 in CD4^(+)T cells in vitro(Pantially inhibited T cell exhaustion and boosted cytokine production by tumor-infiltrating CD8^(+)T cells(Panti-tumor immunity,indicating that PZH holds promise as a potential therapeutic agent for cancer treatment.

关键词： Pien Tze Huang metastasis anti-tumor immunity T cell activation T cell exhaustion immune checkpoints Chinese medicine

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Establishment of NaLuF_(4):15%Tb-based low dose X-PDT agent and its application on efficient antitumor therapy

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International Journal of Minerals,Metallurgy and Materials 2024年第3期31卷 599-610页

作者： Yi Tian Zhiguang Fu Xiaosheng Zhu Chunjing Zhan Jinwei Hu Li Fan Chaojun Song Qian Yang Yu Wang Mei Shi Department of Radiation Oncology Xijing HospitalThe Fourth Military Medical UniversityXi’an 710032China Department of Oncology Air Force Medical CenterPLAThe Fourth Military Medical UniversityBeijing 100142China Department of tumor Radiotherapy Air Force Medical CenterPLAThe Fourth Military Medical UniversityBeijing 100142China Department of Gastroenterology Air Force Hospital of Southern Theater CommandGuangzhou 510062China Department of Pharmaceutical Chemistry and Analysis School of PharmacyThe Fourth Military Medical UniversityXi’an 710032China School of Life Sciences Northwestern Polytechnical UniversityXi’an 710072China Institue of Materia Medica School of PharmacyThe Fourth Military Medical UniversityXi’an 710032China

X-ray excited photodynamic therapy(X-PDT)is the bravo answer of photodynamic therapy(PDT)for deep-seated tumors,as it employs X-ray as the irradiation source to overcome the limitation of light penetration depth.However,high X-ray irradiation dose caused organ lesions and side effects became the major barrier to X-PDT application.To address this issue,this work employed a classic-al co-precipitation reaction to synthesize NaLuF_(4):15%Tb^(3+)(NLF)with an average particle size of(23.48±0.91)nm,which was then coupled with the photosensitizer merocyanine 540(MC540)to form the X-PDT system NLF-MC540 with high production of singlet oxygen.The system could induce antitumor efficacy to about 24%in relative low dose X-ray irradiation range(0.1-0.3 Gy).In vivo,when NLF-MC540 irradiated by 0.1 Gy X-ray,the tumor inhibition percentage reached 89.5%±5.7%.The therapeutic mechanism of low dose X-PDT was found.A significant increase of neutrophils in serum was found on the third day after X-PDT.By immunohistochemical staining of tumor sections,the Ly6G^(+),CD8^(+),and CD11c^(+)cells infiltrated in the tumor microenvironment were studied.Utilizing the bilat-eral tumor model,the NLF-MC540 with 0.1 Gy X-ray irradiation could inhibit both the primary tumor and the distant tumor growth.De-tected by enzyme linked immunosorbent assay(ELISA),two cytokines IFN-γand TNF-αin serum were upregulated 7 and 6 times than negative control,respectively.Detected by enzyme linked immune spot assay(ELISPOT),the number of immune cells attributable to the IFN-γand TNF-αlevels in the group of low dose X-PDT were 14 and 6 times greater than that in the negative control group,respectively.Thus,it conclude that low dose X-PDT system could successfully upregulate the levels of immune cells,stimulate the secretion of cy-tokines(especially IFN-γand TNF-α),activate antitumor immunity,and finally inhibit colon tumor growth.

关键词： X-ray excited photodynamic therapy singlet oxygen low dose X-Ray irradiation efficient antitumor therapy anti-tumor immunity

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anti-tumor immunity of BAM-SiPc-mediated vascular photodynamic therapy in a BALB/c mouse model

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Cellular & Molecular Immunology 2017年第2期14卷 223-234页

作者： Hing-Yuen Yeung Pui-Chi Lo Dennis K.P. Ng Wing-Ping Fong School of Life Sciences The Chinese University of Hong Kong Shatin N.T. Hong Kong China Department of Biomedical Sciences City University of Hong Kong Tat Chee Avenue Kowloon Hong Kong China Department of Chemistry The Chinese University of Hong Kong Shatin N.T. Hong Kong China

In recent decades, accumulating evidence from both animal and clinical studies has suggested that a sufficiently activated immune system may strongly augment various types of cancer treatment, including photodynamic therapy （PDT）. Through the generation of reactive oxygen species, PDT eradicates tumors by triggering localized tumor damage and inducing anti-tumor immunity. As the major component of anti-tumor immunity, the involvement of a cell-mediated immune response in PDT has been well investigated in the past decade, whereas the role of humoral immunity has remained relatively unexplored. In the present investigation, using the photosensitizer BAM-SiPc and the CT26 tumor-bearing BALB/c mouse model, it was demonstrated that both cell-mediated and humoral adaptive immune components could be involved in PDT. With a vascular PDT （VPDT） regimen, BAM-SiPc could eradicate the tumors of -70% of tumor-bearing mice and trigger an anti-tumor immune response that could last for more than 1 year. An elevation of Th2 cytokines was detected ex vivoafter VPDT, indicating the potential involvement of a humoral response. An analysis of serum from the VPDT-cured mice also revealed elevated levels of tumor-specific antibodies. Moreover, this serum could effectively hinder tumor growth and protect the mice against further re-challenge in a T-cell-dependent manner. Taken together, these results show that the humoral components induced after BAM-SiPc-VPDT could assist the development of anti-tumor immunity.

关键词： anti-tumor immunity damage-associated molecular patterns humoral immunity photodynamic therapy tumor-bearing mice

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Radiofrequency ablation,heat shock protein 70 and potential anti-tumor immunity in hepatic and pancreatic cancers:a minireview

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Hepatobiliary & Pancreatic Diseases International 2010年第4期9卷 361-365页

作者： Teng, Li-Song Jin, Ke-Tao Han, Na Cao, Jiang Zhejiang Univ Sch Med Ctr Canc Affiliated Hosp 1 Hangzhou 310003 Zhejiang Peoples R China Zhejiang Univ Sir Run Run Shaw Inst Clin Med Key Lab Biotherapy Zhejiang Prov Hangzhou 310016 Zhejiang Peoples R China

BACKGROUND: Radiofrequency ablation (RFA) is a minimally invasive surgical procedure which has widespread popularity in the treatment of hepatic and pancreatic cancers. Increased evidence indicates that RFA stimulates anti-tumor immunity, possibly through the induction heat shock protein 70 (HSP70) expression. HSP70 has the capacity to affect the immunogenicity of tumor cells, to chaperone antigenic peptides and deliver these into antigen presentation pathways within antigen-presenting cells, and to activate and regulate innate and adaptive immunity, which makes it useful in immunotherapeutic strategies for the treatment of cancers. DATA SOURCES: An English-language literature search was conducted using MEDLINE (1991-2010) on anti-tumor immunity, heat shock protein 70, radiofrequency ablation, hepatic cancer, pancreatic cancer, and other related subjects. RESULTS: RFA has an increasing application in the surgical treatment of hepatic and pancreatic cancers. Increased evidence indicates that RFA can induce the expression of HSP70 which possesses properties that enable it to influence a variety of immunological processes. tumor-derived HSP70 is regarded as a potent adjuvant facilitating presentation of tumor antigens and induction of anti-tumor immunity. CONCLUSIONS: This review addresses the potential association of RFA, HSP70, and anti-tumor immunity in treatment of hepatic and pancreatic cancers. To establish direct evidence of a potential association of RFA, HSP70, and anti-tumor immunity in hepatic and pancreatic cancers, further investigations should be conducted.

关键词： anti-tumor immunity heat shock protein 70 hepatic cancer pancreatic cancer radiofrequency ablation

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Gene Therapy of Cancer:Induction of anti-tumor immunity

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Cellular & Molecular Immunology 2004年第2期1卷 105-111页

作者： Jesus Prieto Division

Many malignancies lack satisfactory treatment and new therapeutic options are urgently needed.Gene therapy is a new modality to treat both inherited and acquired diseases based on the transfer of genetic material to the tissues.Different gene therapy strategies against cancers have been developed.A considerable number of preclinical studies indicate that a great variety of cancers are amenable to gene therapy.Among these strategies, induction of anti-tumor immunity is the most promising approach.Gene therapy with cytokines has reached unprecedented success in preclinical models of cancer.Synergistic rather than additive effects have been demonstrated by combination of gene transfer of cytokines/chemokines,costimulatory molecules or adoptive cell therapy.Recent progress in vector technology and in imaging techniques allowing in vivo assessment of gene expression will facilitate the development of clinical applications of gene therapy,a procedure which may have a notorious impact in the management of cancers lacking effective treatment.Cellular & Molecular Immunology.2004;1(2):105-111.

关键词： gene therapy anti-tumor immunity cytokines costimulatory molecules dendritic cell

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Tetrahedral DNA nanostructures synergize with MnO_(2) to enhance antitumor immunity via promoting STING activation and M1 polarization

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Acta Pharmaceutica Sinica B 2022年第5期12卷 2494-2505页

作者： Siping Liang Jiaying Li Zhengyu Zou Miao Mao Siqi Ming Fan Lin Ziyan Zhang Can Cao Jinyu Zhou Yuanqing Zhang Jiaping Li Minhao Wu Zhongshan School of Medicine Sun Yat-sen UniversityGuangzhou 510080China Department of Laboratory Medicine Guangdong Second Provincial General HospitalGuangzhou 510317China Guangdong Key Laboratory of Chiral Molecule and Drug Discovery School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510006China Department of Interventional Oncology The First Afﬁliated HospitalSun Yat-sen UniversityGuangzhou 510080China

Stimulator of interferon genes(STING) is a cytosolic DNA sensor which is regarded as a potential target for antitumor immunotherapy. However, clinical trials of STING agonists display limited anti-tumor effects and dose-dependent side-effects like inflammatory damage and cell toxicity. Here,we showed that tetrahedral DNA nanostructures(TDNs) actively enter macrophages to promote STING activation and M1 polarization in a size-dependent manner, and synergized with Mn^(2+) to enhance the expressions of IFN-β and iNOS, as well as the co-stimulatory molecules for antigen presentation. Moreover, to reduce the cytotoxicity of Mn^(2+),we constructed a TDN-MnO_(2) complex and found that it displayed a much higher efficacy than TDN plus Mn^(2+) to initiate macrophage activation and anti-tumor response both in vitro and in vivo. Together, our studies explored a novel immune activation effect of TDN in cancer therapy and its synergistic therapeutic outcomes with MnO_(2).These findings provide new therapeutic opportunities for cancer therapy.

关键词： Tetrahedral DNA nanostructure Manganese MnO_(2) STING M1 polarization antigen presentation anti-tumor immunity Cancer therapy

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Metabolic regulation of immune responses to cancer

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Cancer Biology & Medicine 2022年第11期19卷 1528-1542页

作者： Jannis WiBfeld Anke Werner Xin Yan Nora ten Bosch Guoliang Cui Helmholtz Institute for Translational Oncology(HI-TRON) Mainz 55131Germany T Cell Metabolism Group(D192) German Cancer Research Center(DKFZ)Heidelberg 69120Germany Faculty of Biosciences Heidelberg UniversityHeidelberg 69120Germany

The tumor microenvironment is an ecosystem composed of multiple types of cells, such as tumor cells, immune cells, and cancerassociated fibroblasts. Cancer cells grow faster than non-cancerous cells and consume larger amounts of nutrients. The rapid growth characteristic of cancer cells fundamentally alters nutrient availability in the tumor microenvironment and results in reprogramming of immune cell metabolic pathways. Accumulating evidence suggests that cellular metabolism of nutrients, such as lipids and amino acids, beyond being essential to meet the bioenergetic and biosynthetic demands of immune cells, also regulates a broad spectrum of cellular signal transduction, and influences immune cell survival, differentiation, and anti-tumor effector function. The cancer immunometabolism research field is rapidly evolving, and exciting new discoveries are reported in high-profile journals nearly weekly. Therefore, all new findings in this field cannot be summarized within this short review. Instead, this review is intended to provide a brief introduction to this rapidly developing research field, with a focus on the metabolism of two classes of important nutrients-lipids and amino acids-in immune cells. We highlight recent research on the roles of lipids and amino acids in regulating the metabolic fitness and immunological functions of T cells, macrophages, and natural killer cells in the tumor microenvironment. Furthermore, we discuss the possibility of “editing” metabolic pathways in immune cells to act synergistically with currently available immunotherapies in enhancing anti-tumor immune responses.

关键词： Lipids amino acids cancer anti-tumor immunity T cells NK cells metabolism immunometabolism

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Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation

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Cellular & Molecular Immunology 2023年第10期20卷 1127-1139页

作者： Yubing Fu Jinjia Wang Chenfeng Liu Kunyu Liao Xianjun Gao Ronghan Tang Binbin Fan Yazhen Hong Nengming Xiao Changchun Xiao Wen-Hsien Liu State Key Laboratory of Cellular Stress Biology School of Life SciencesFaculty of Medicine and Life ScienceXiamen UniversityXiamen361102FujianChina Department of Cell Biology School of Life ScienceAnhui Medical UniversityHefei230031AnhuiChina Sanof institute for Biomedical Research SuzhouJiangsu 215123 China.

Cellular immunity mediated by CD8+T cells plays an indispensable role in bacterial and viral clearance and cancers.However,persistent antigen stimulation of CD8+T cells leads to an exhausted or dysfunctional cellular state characterized by the loss of effector function and high expression of inhibitory receptors during chronic viral infection and in tumors.Numerous studies have shown that glycogen synthase kinase 3(GSK3)controls the function and development of immune cells,but whether GSK3 affects CD8+T cells is not clearly elucidated.Here,we demonstrate that mice with deletion of Gsk3αand Gsk3βin activated CD8+T cells(DKO)exhibited decreased CTL differentiation and effector function during acute and chronic viral infection.In addition,DKO mice failed to control tumor growth due to the upregulated expression of inhibitory receptors and augmented T-cell exhaustion in tumor-infiltrating CD8+T cells.Strikingly,anti-PD-1 immunotherapy substantially restored tumor rejection in DKO mice.Mechanistically,GSK3 regulates T-cell exhaustion by suppressing TCR-induced nuclear import of NFAT,thereby in turn dampening NFAT-mediated exhaustion-related gene expression,including TOX/TOX2 and PD-1.Thus,we uncovered the molecular mechanisms underlying GSK3 regulation of CTL differentiation and T-cell exhaustion in anti-tumor immune responses.

关键词： GSK3 T-cell exhaustion Viral infection anti-tumor immunity Inhibitory receptors

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