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Black phosphorus-based photothermal therapy with aCD47-mediated immune checkpoint blockade for enhanced cancer immunotherapy

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Light(Science & Applications) 2020年第1期9卷 479-493页

作者： Zhongjian Xie Minhua Peng Ruitao Lu Xiangying Meng Weiyuan Liang Zhongjun Li Meng Qiu Bin Zhang Guohui Nie Ni Xie Han Zhang Paras N.Prasad Shenzhen International Institute for Biomedical Research Shenzhen 518116 GuangdongPR China Shenzhen Institutes of Advanced Technology Chinese Academy of SciencesShenzhen 518055 GuangdongPR China School of Basic Medical Sciences Guangzhou Medical UniversityGuangzhou 511436 GuangdongPR China Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province Institute of Microscale Optoelectronicsand Otolaryngology Department and Biobank of the First Affiliated HospitalShenzhen Second People’s HospitalHealth Science CenterShenzhen UniversityShenzhen 518060PR China Key Laboratory of Marine Chemistry Theory and Technology(Ocean University of China) Ministry of EducationQingdao 266100PR China Department of Chemistry Institute for LasersPhotonicsand BiophotonicsUniversity at BuffaloStateUniversity of New YorkBuffaloNYUSA

Here,we describe a combination strategy of black phosphorus(BP)-based photothermal therapy together with anti-CD47 antibody(aCD47)-based immunotherapy to synergistically enhance cancer *** resistance to immune checkpoint blockades in most cancers due to immune escape from host surveillance,along with the initiation of metastasis through immunosuppressive cells in the tumour microenvironment,remains a significant challenge for cancer ***47,an agent for CD47/SIRPαaxis blockade,induces modest phagocytic activity and a low response rate for monotherapy,resulting in failures in clinical *** showed that BP-mediated ablation of tumours through photothermal effects could serve as an effective strategy for specific immunological stimulation,improving the inherently poor immunogenicity of tumours,which is particularly useful for enhancing cancer *** in combination with aCD47 blockade activates both innate and adaptive immunities and promotes local and systemic anticancer immune responses,thus offering a synergistically enhanced effect in suppression of tumour progression and in inducing abscopal effects for inhibition of metastatic *** combination strategy provides a promising platform in which photothermal agents could help to enhance the therapeutic efficacy of immunotherapy.

关键词： immunotherapy cancer mediated

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m6A RNA methylation-mediated HNF3γ reduction rendershepatocellular carcinoma dedifferentiation and sorafenibresistance

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Signal Transduction and Targeted Therapy 2021年第1期6卷 144-157页

作者： Tengfei Zhou Shichao Li Daimin Xiang Junyu Liu Wen Sun Xiuliang Cui Beifang Ning Xiao Li Zhuo Cheng Weiqi Jiang Cheng Zhang Xijun Liang Liang Li Xin Cheng Liu Hui Hongyang Wang Jin Ding International Cooperation Laboratory on Signal Transduction Eastern Hepatobiliary Surgery Hospital/InstituteThe Second Military Medical UniversityShanghaiChina Department of Gastroenterology Changzheng HospitalThe Second Military Medical UniversityShanghaiChina Shanghai Institutes for Biological Sciences Chinese Academy of SciencesShanghaiChina The Third Department of Hepatic Surgery Eastern Hepatobiliary Surgery HospitalThe Second Military Medical UniversityShanghaiChina National Center for Liver Cancer ShanghaiChina Tongji University School of Medicine ShanghaiChina

Hepatocyte nuclear factor 3γ(HNF3γ)is a hepatocyte nuclear factor,but its role and clinical significance in hepatocellular carcinoma(HCC)remain ***,we report that HNF3γexpression is downregulated in patient HCC and inversely correlated with HCC malignancy and patient ***,our data suggested that the HNF3γreduction in HCC could be mediated by METTL14-dependent m6A methylation of HNF3γ***3γexpression was increased during hepatic differentiation and decreased in dedifferentiated HCC ***,HNF3γdelivery promoted differentiation of not only HCC cells but also liver CSCs,which led to suppression of HCC *** analysis suggested an HNF3γ-centered regulatory network that includes essential liver differentiation-associated transcription factors and functional molecules,which could synergistically facilitate HCC cell *** importantly,enforced HNF3γexpression sensitized HCC cells to sorafenib-induced growth inhibition and cell apoptosis through transactivation of OATP1B1 and OATP1B3 expression,which are major membrane transporters for sorafenib *** investigation showed that patient-derived HCC xenografts with high HNF3γexpression exhibited a sorafenib response and patients with high HCC HNF3γlevels benefited from sorafenib ***,these results suggest that HNF3γplays an essential role in HCC differentiation and may serve as a therapeutic target and predictor of sorafenib benefit in patients.

关键词： sorafenib hepatocellular mediated

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Estrogen-mediated downregulation of HIF-1αsignaling in B lymphocytes influences postmenopausal bone loss

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Bone Research 2022年第2期10卷 326-337页

作者： Xianyi Meng Zhen Lin Shan Cao Iga Janowska Koshiro Sonomoto Darja Andreev Knab Katharina Jinming Wen Karl Xaver Knaup Michael Sean Wiesener Gerhard Krönke Marta Rizzi Georg Schett Aline Bozec Department of Internal Medicine 3 Friedrich-Alexander-University Erlangen-Nürnberg(FAU)and Universitätsklinikum ErlangenErlangen 91054Germany Deutsches Zentrum fur Immuntherapie(DYI) Erlangen 91054Germany Department of Rheumatology and Clinical Immunology Faculty of MedicineMedical Center-University of FreiburgFreiburg 79106Germany Department of Internal Medicine 4 Friedrich-Alexander-University Erlangen-Nürnberg(FAU)and Universitätsklinikum ErlangenErlangen 91054Germany

In the bone marrow, B cells and bone-resorbing osteoclasts colocalize and form a specific microenvironment. How B cells functionally influence osteoclasts and bone architecture is poorly understood. Using genetically modified mice and highthroughput analyses, we demonstrate that prolonged HIF-1α signaling in B cells leads to enhanced RANKL production and osteoclast formation. In addition, deletion of HIF-1α in B cells prevents estrogen deficiency-induced bone loss in ***, estrogen controls HIF-1α protein stabilization through HSP70-mediated degradation in bone marrow B *** stabilization of HIF-1α protein in HSP70-deficient bone marrow B cells promotes RANKL production and *** of HSP70 expression by geranylgeranylacetone(GGA) administration alleviates ovariectomy-induced ***, RANKL gene expression has a positive correlation with HIF1 A expression in human B cells. In conclusion, HIF-1αsignaling in B cells is crucial for the control of osteoclastogenesis, and the HSP70/HIF-1α axis may serve as a new therapeutic target for osteoporosis.

关键词： mediated lymphocytes stabilization

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Development of a Haploid-Inducer mediated Genome Editing System for Accelerating Maize Breeding

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Molecular Plant 2019年第4期12卷 597-602页

作者： Baobao Wang Lei Zhu Binbin Zhao Yongping Zhao Yurong Xie Zhigang Zheng Yaoyao Li Juan Sun Haiyang Wang Biotechnology Research Institute Chinese Academy of Agricultural Sciences Beijing 100081 China School of Life Sciences State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources South China Agricultural University Guangzhou 510642 China

Crop breeding aims to generate pure in bred lines with multiple desired traits. Doubled haploid (DH) and genome editing using CRISPR/Cas9 are two powerful game-changing technologies in crop breeding. However, both of them still fall short for rapid generation of pure elite lines with integrated favorable traits. Here, we report the development of a Haploid-Inducer mediated Genome Editing (IMGE) approach, which utilizes a maize haploid inducer line carrying a CRISPR/Cas9 cassette targeting for a desired agronomic trait to pollinate an elite maize in bred line and to generate genome-edited haploids in the elite maize background. Homozygous pure DH lines with the desired trait improvement could be generated within two generations, thus bypassing the lengthy procedure of repeated crossing and backcrossing used in conventional breeding for integrating a desirable trait into elite commercial backgrounds.

关键词： maize, doubled haploids (DH) CRSIPR/Cas9 haploid-inducer mediated genome editing (IMGE) crop breeding

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Mechanical tibial loading remotely suppresses brain tumors by dopamine-mediated downregulation of CCN4

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Bone Research 2021年第3期9卷 313-322页

作者： Yao Fan Rongrong Zha Tomohiko Sano Xinyu Zhao Shengzhi Liu Mark D.Woollam Di Wu Xun Sun Kexin Li Motoki Egi Fangjia Li Kazumasa Minami Amanda P.Siegel Takashi Horiuchi Jing Liu Mangilal Agarwal Akihiro Sudo Harikrishna Nakshatri Bai-Yan Li Hiroki Yokota Department of Phamacology School of PharmacyHarbin Medical UniversityHarbinChina Department of Biomedical Engineering Indiana University Purdue University IndianapolisIndianapolisIndianaUSA Department of Orthopedic Surgery Mie UniversityMieJapan Peking Union Medical College Hospital Chinese Academy of Medical SciencesBeijingChina Department of Chemistry and Chemical Biology Indiana University Purdue University IndianapolisIndianapolisINUSA Integrative Nanosystems Development Institute Indiana University Purdue University IndianapolisIndianapolisINUSA Graduate School of Engineering Mie UniversityMieJapan Department of Physics Indiana University Purdue University IndianapolisIndianapolisINUSA Department of Radiation Oncology Osaka University Graduate School of MedicineSuitaOsakaJapan Simon Cancer Center Indiana University School of MedicineIndianapolisINUSA Department of Surgery Simon Cancer Research CenterIndiana University School of MedicineIndianapolisINUSA

Mechanical loading to the bone is known to be beneficial for bone homeostasis and for suppressing tumor-induced osteolysis in the loaded ***,whether loading to a weight-bearing hind limb can inhibit distant tumor growth in the brain is *** examined the possibility of bone-to-brain mechanotransduction using a mouse model of a brain tumor by focusing on the response to Lrp5-mediated Wnt signaling and dopamine in tumor *** results revealed that loading the tibia with elevated levels of tyrosine hydroxylase,a rate-limiting enzyme in dopamine synthesis,markedly reduced the progression of the brain *** simultaneous application of fluphenazine(FP),an antipsychotic dopamine modulator,enhanced tumor *** and FP exerted antitumor effects through the dopamine receptors DRD1 and DRD2,***,dopamine downregulated Lrp5 via DRD1 in tumor cells.A cytokine array analysis revealed that the reduction in CCN4 was critical for loading-driven,dopamine-mediated tumor *** silencing of Lrp5 reduced CCN4,and the administration of CCN4 elevated oncogenic genes such as MMP9,Runx2,and *** summary,this study demonstrates that mechanical loading regulates dopaminergic signaling and remotely suppresses brain tumors by inhibiting the Lrp5-CCN4 axis via DRD1,indicating the possibility of developing an adjuvant bone-mediated loading therapy.

关键词： dopamine mediated elevated

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Macrophage-derived small extracellular vesicles promote biomimetic mineralized collagen-mediated endogenous bone regeneration

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International Journal of Oral Science 2020年第4期12卷 317-326页

作者： Anqi Liu Shanshan Jin Cuicui Fu Shengji Cui Ting Zhang Lisha Zhu Yu Wang Steve G.F.Shen Nan Jiang Yan Liu Department of Oral and Maxillofacial Surgery Ninth People’s HospitalShanghai Jiao Tong University School of MedicineShanghai Key Laboratory of StomatologyShanghaiChina Laboratory of Biomimetic Nanomaterials Department of OrthodonticsPeking University School and Hospital of StomatologyNational Engineering Laboratory for Digital and Material Technology of StomatologyBeijing Key Laboratory of Digital StomatologyBeijingChina Department of Oral Biochemistry Academic Centre for Dentistry Amsterdam(ACTA)University of Amsterdam(UvA)and Vrije Universiteit Amsterdam(VU)Gustav Mahlerlaan 3004AmsterdamThe Netherlands Shanghai University of Medicine and Health Sciences ShanghaiChina Central Laboratory Peking University School and Hospital of StomatologyNational Engineering Laboratory for Digital and Material Technology of StomatologyBeijing Key Laboratory of Digital StomatologyBeijingChina

Macrophages play an important role in material-related immune responses and bone formation,but the functionality of macrophage-derived extracellular vesicles(EVs)in material-mediated bone regeneration is still ***,we evaluated intracellular communication through small extracellular vesicles(sEVs)and its effects on endogenous bone regeneration mediated by biomimetic intrafibrillarly mineralized collagen(IMC).After implantation in the bone defect area,IMC generated more neobone and recruited more mesenchymal stem cells(MSCs)than did extrafibrillarly mineralized collagen(EMC).More CD63+CD90+and CD63+CD163+cells were detected in the defect area in the IMC group than in the EMC *** determine the functional roles of sEVs,extracellular vesicles from macrophages cultured on different mineralized collagen were isolated,and they showed no morphological ***,macrophage-derived sEVs in the IMC group showed an enhanced Young’s modulus and exerted beneficial effects on the osteogenic differentiation of bone marrow MSCs by increasing the expression of the osteoblastic differentiation markers BMP2,BGLAP,COL1,and OSX and calcium nodule ***,sEVs from IMC-treated macrophages facilitated MSC osteogenesis through the BMP2/Smad5 pathway,and blocking sEV secretion with GW4869 significantly impaired MSC proliferative,immunomodulative and osteogenic *** together,these findings show that macrophage-derived sEVs may serve as an emerging functional tool in biomaterial-mediated endogenous bone regeneration.

关键词： endogenous CD63 mediated

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METTL7A-mediated m6A modification of corin reverses bisphosphonates-impaired osteogenic differentiation of orofacial BMSCs

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International Journal of Oral Science 2024年第3期16卷 528-538页

作者： Yizhou Jin Xiao Han Yuejun Wang Zhipeng Fan Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Beijing Stomatological HospitalSchool of StomatologyCapital Medical UniversityBeijingChina Beijing Laboratory of Oral Health Capital Medical UniversityBeijingChina Research Unit of Tooth Development and Regeneration Chinese Academy of Medical SciencesBeijingChina

Bisphosphonate-related osteonecrosis of jaw(BRONJ)is characterized by impaired osteogenic differentiation of orofacial bone marrow stromal cells(BMSCs).Corin has recently been demonstrated to act as a key regulator in bone development and orthopedic ***,the role of corin in BRONJ-related BMSCs dysfunction remains unclarified.A m6A epitranscriptomic microarray study from our group shows that the CORIN gene is significantly upregulated and m6A hypermethylated during orofacial BMSCs osteogenic *** knockdown inhibits BMSCs osteogenic differentiation,whereas corin overexpression or soluble corin(sCorin)exerts a promotion ***,corin expression is negatively regulated by bisphosphonates(BPs).Corin overexpression or sCorin reverses BPs-impaired BMSCs differentiation ***,we find altered expression of phos-ERK in corin knockdown/overexpression BMSCs and BMSCs under sCorin ***98059(a selective ERK inhibitor)blocks the corin-mediated promotion *** regard to the high methylation level of corin during osteogenic differentiation,we apply a non-selective m6A methylase inhibitor,Cycloleucine,which also blocks the corin-mediated promotion ***,we demonstrate that METTL7A modulates corin m6A modification and reverses BPs-impaired BMSCs function,indicating that METTL7A regulates corin expression and thus contributes to orofacial BMSCs differentiation *** conclude,our study reveals that corin reverses BPs-induced BMSCs dysfunction,and METTL7A-mediated corin m6A modification underlies corin promotion of osteogenic differentiation via the ERK *** hope this brings new insights into future clinical treatments for BRONJ.

关键词： impaired cor mediated

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Eating self for not be eaten:Pancreatic cancer suppresses selfimmunogenicity by autophagy-mediated MHC-I degradation

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1626-1627页

作者： Xing Huang Xiaozhen Zhang Xueli Bai Tingbo Liang Zhejiang Provincial Key Laboratory of Pancreatic Disease the First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310003 ZhejiangChina Department of Hepatobiliary and Pancreatic Surgery the First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310003 ZhejiangChina

In a recent study in Nature,1 Yamamoto et *** that MHC-I is a selective substrate of autophagy in tumor immune ***,it was reported that autophagy-mediated lysosomal degradation of MHC-I suppresses pancreatic cancer immunogenicity and the effectiveness of *** findings indicate the potential of autophagy inhibition as a strategy to activate anti-pancreatic cancer immunity.

关键词： cancer al mediated

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Pancreatic cancer cells render tumor-associated macrophages metabolically reprogrammed by a GARP and DNA methylation-mediated mechanism

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Signal Transduction and Targeted Therapy 2021年第11期6卷 3348-3365页

作者： Mengwen Zhang Xingyi Pan Kenji Fujiwara Noelle Jurcak Stephen Muth Jiaojiao Zhou Qian Xiao Anqi Li Xu Che Zihai Li Lei Zheng Department of Oncology Johns Hopkins University School of MedicineBaltimoreMD21287USA The Sidney Kimmel Cancer Center Johns Hopkins University School of MedicineBaltimoreMD21287USA The Pancreatic Cancer Precision Medicine Center of Excellence Program Johns Hopkins University School of MedicineBaltimoreMD21287USA The Cellular and Molecular Medicine Graduate Program Johns Hopkins University School of MedicineBaltimoreMD21287USA Pelotonia Institute for Immune-Oncology The Ohio State University Comprehensive Cancer CenterColumbusOH43210USA Department of Surgery Johns Hopkins University School of MedicineBaltimoreMD21287USA The Second Affiliated Hospital Zhejiang University School of MedicineHangzhouChina Department of Surgery Sada HospitalFukuokaJapan Cancer Hospital Chinese Academy of Medical SciencesShenzhenChina

How tumor-associated macrophages transit from a predominant antitumor M1-like phenotype to a protumoral M2-like phenotype during the development of pancreatic ductal adenocarcinoma (PDA) remains to be elucidated. We thus conducted a study by employing a PDA-macrophage co-culture system, an “orthotopic” PDA syngeneic mouse model, and human PDA specimens, together with macrophages derived from GARP knockout mice and multiple analytic tools including whole-genome RNA sequencing, DNA methylation arrays, multiplex immunohistochemistry, metabolism measurement, and invasion/metastasis assessment. Our study showed that PDA tumor cells, through direct cell–cell contact, induce DNA methylation and downregulation of a panel of glucose metabolism and OXPHOS genes selectively in M1-like macrophages, leading to a suppressed glucose metabolic status in M1-like but not in M2-like macrophages. Following the interaction with PDA tumor cells, M1-like macrophages are reprogrammed phenotypically to M2-like macrophages. The interaction between M1-like macrophages and PDA cells is mediated by GARP and integrin αV/β8, respectively. Blocking either GARP or integrin would suppress tumor-induced DNA methylation in Nqo-1 gene and the reprogramming of M1-like macrophages. Glucose-response genes such as Il-10 are subsequently activated in tumor-educated M1-like macrophages. Partly through Il-10 and its receptor Il-10R on tumor cells, M1-like macrophages functionally acquire a pro-cancerous capability. Both exogenous M1-like and M2-like macrophages promote metastasis in a mouse model of PDA while such a role of M1-like macrophages is dependent on DNA methylation. Our results suggest that PDA cells are able to reprogram M1-like macrophages metabolically and functionally through a GARP-dependent and DNA methylation-mediated mechanism to adopt a pro-cancerous fate.

关键词： metabolism metastasis mediated

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TRAF3 activates STING-mediated suppression of EV-A71 and target of viral evasion

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Signal Transduction and Targeted Therapy 2023年第3期8卷 1296-1309页

作者： Wenwen Zheng Zhenbang Zhou Yajuan Rui Runxin Ye Fengyan Xia Fei Guo Xiaoman Liu Jiaming Su Meng Lou Xiao-Fang Yu Cancer Institute(Key Laboratory of Cancer Prevention and Intervention China National Ministry of Education)The Second Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310009China National Health Commission of the People’s Republic of China Key Laboratory of Systems Biology of Pathogens Institute of Pathogen Biology and Center for AIDS ResearchChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Cancer Center Zhejiang UniversityHangzhouZhejiang 310058China

Innate immunity represents one of the main host responses to viral infection.1,2,3 STING(Stimulator of interferon genes),a crucial immune adapter functioning in host cells,mediates cGAS(Cyclic GMP-AMP Synthase)sensing of exogenous and endogenous DNA fragments and generates innate immune responses.4 Whether STING activation was involved in infection and replication of enterovirus remains largely *** the present study,we discovered that human enterovirus A71(EV-A71)infection triggered STING activation in a cGAS dependent ***-A71 infection caused mitochondrial damage and the discharge of mitochondrial DNA into the cytosol of infected ***,during EV-A71 infection,cGAS-STING activation was ***-A71 ^(pro)teins were screened and the viral ^(pro)tease 2A^(pro) had the greatest capacity to inhibit cGAS-STING *** identified TRAF3 as an important factor during STING activation and as a target of 2A^(pro).Supplement of TRAF3 rescued cGAS-STING activation suppression by 2A^(pro).TRAF3 supported STING activation mediated TBK1 ***,we found that 2A^(pro) ^(pro)tease activity was essential for inhibiting STING ***,EV-D68 and CV-A16 infection also triggered STING *** viral ^(pro)tease 2A^(pro) from EV-D68 and CV-A16 also had the ability to inhibit STING *** STING activation prior to EV-A71 infection generated cellular resistance to EV-A71 replication,blocking EV-A71-mediated STING suppression represents a new anti-viral target.

关键词： mediated TRAF3 immunity

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