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Intra-heterogeneity in transcription and chemoresistant property of leukemia-initiating cells in murine Setd2^(-/-) acutemyeloid leukemia

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cancer Communications 2021年第9期41卷 867-888页

作者： Jiachun Song Longting Du Ping Liu Fuhui Wang Bo Zhang Yinyin Xie Jing Lu Yi Jin Yan Zhou Gang Lv Jianmin Zhang Saijuan Chen Zhu Chen Xiaojian Sun Yuanliang Zhang Qiuhua Huang Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiRuijin Hospital affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025P.R.China Novel Bioinformatics Co. LtdShanghai 201114P.R.China Central Laboratory Renji Hospital affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200127P.R.China

Background:Heterogeneity of leukemia-initiating cells(LICs)is a major obstacle in acute myeloid leukemia(AML)*** evidence indicates that the coexistence of multiple types of LICs with different pathogenicity in the same individual is a common feature in ***,the functional heterogeneity including the drug response of coexistent LICs remains ***,this study aimed to clarify the intra-heterogeneity in LICs that can help predict leukemia behavior and develop more effective ***:Spleen cells from the primary Setd2^(-/-)-AML mouse were transplanted into C57BL/6 recipient mice to generate a transplantable *** cytometry was used to analyze the immunophenotype of the leukemic ***-genome sequencing was conducted to detect secondary hits responsible for leukemia transformation.A serial transplantation assay was used to determine the self-renewal potential of Setd2^(-/-)-AML cells.A limiting-dilution assay was performed to identify the LIC frequency in different subsets of leukemia *** and single-cell RNA sequencing were performed to analyze the transcriptional heterogeneity of *** molecular inhibitor screening and in vivo drug treatment were employed to clarify the difference in drug response between the different subsets of ***:In this study,we observed an aged Setd2^(-/-)mouse developing AML with co-mutation of Nras^(G12S) and Braf^(K520E).Further investigation identified two types of LICs residing in the c-Kit^(+)B220^(+)Mac-1^(-)and c-Kit^(+)B220^(+)Mac-1^(+)subsets,*** vivo transplantation assay disclosed the heterogeneity in differentiation between the coexistent ***,an intrinsic doxorubicinresistant transcriptional signature was uncovered in c-Kit^(+)B220^(+)Mac-1^(+)***,doxorubicin plus cytarabine(DA),the standard chemotherapeutic regimen used in AML treatment,could specifically kill c-Kit^(+)B220^(+)Mac-1^(−)cells,but it hardly affected c-Kit^(+)B220^(

关键词： heterogeneity leukemia-initiating cell Setd2−/−acute myeloid leukemia single-cell RNA sequencing drug response

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Zfyve16 regulates the proliferation of β-lymphoid cells

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Frontiers of Medicine 2018年第5期12卷 559-565页

作者： Xuemei Zhao Donghe Li Qingsong Qiu Bo Jiao Ruihong Zhang Ping Liu Ruibao Ren State Key Laboratory for Medical Genomics Shanghai Institute of Hematology Collaborative Innovation Center of HematologyCollaborative Innovation Center of System Biology Ruo'in Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai200025 China Department of Biology Brandeis University Waltham MA 02454 USA

Zfyve16 (a.k.a. endofin or endosome-associated FYVE-domain protein), a member of the FYVE-domain protein family, is involved in endosomal trafficking and in TGF-β, BMP, and EGFR signaling. The FYVE protein SARA regulates the TGF-β signaling pathway by recruiting Smad2/3 and accelerating their phosphorylation, thereby altering their susceptibility to TGF-β-mediated T cell suppression. Zfyve16 binds to Smad4 and their binding affects the formation of Smad2/3-Smad4 complex in TGF-β signaling. However, the in vivo function of Zfyve16 remains unknown. In this study, we generated a Zfyve16 knockout mouse strain (Zfyve16KO) and examined its hematopoietic phenotypes and hematopoietic reconstruction ability. The proportion of Tcells in the peripheral blood of Zfyve16KO mice increases compared with that in wild-type mice. This finding is consistent with the role of Zfyve16 in facilitating TGF-β signaling. Unpredictably, B cell proliferation is inhibited in Zfyve16KO mice. The proliferation potential of Zfyve16KO B-lymphoid cells also significantly decreases in vitro. These results suggest that Zfyve16 inhibits the proliferation of T cells, possibly through the TGF-β signaling, but upregulates the proliferation of B-lymphoid cells.

关键词： TGF-β Zfyve16 endofin hematopoiesis lymphocytes

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Inhibition of the nuclear export of p65 and IQCG in leukemogenesis by NUP98-IQCG

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Frontiers of Medicine 2016年第4期10卷 410-419页

作者： Mengmeng Pan Qiyao Zhang Ping Liu Jinyan Huang YueyingWang Saijuan Chen State Key Laboratory of Medical Genomics Shanghai Institute of Hematology Rui Jin Hospital Affiliated to Shanghai Jiao Tong University (SJTU) School of Medicine Shanghai 200025 China Institute of Health Sciences Shanghai Institutes for Biological Sciences and Graduate School Chinese Academy of Sciences and SJTU School of Medicine Shanghai 200025 China

NUP98 fuses with approximately 34 different partner genes via translocation in hematological malignancies. Transgenic or retrovirus-mediated bone marrow transplanted mouse models reveal the leukemogenesis of some NUP98-related fusion genes. We previously reported the fusion protein NUP98-IQ motif containing G （IQCG） in a myeloid/T lymphoid bi-phenoleukemia patient with t（3;11） and confirmed its leukemogenic ability. Herein, we demonstrated the association of NUP98-IQCG with CRM1, and found that NUP98-IQCG expression inhibits the CRMl-mediated nuclear export of p65 and enhances the transcriptional activity of nuclear factor-κB. Moreover, IQCG could be entrapped in the nucleus by NUP98-IQCG, and the fusion protein interacts with calmodulin via the IQ motif in a calcium-independent manner. Therefore, the inhibition of nuclear exports of p65 and IQCG might contribute to the leukemogenesis of NUP98-IQCG.

关键词： NUP98-IQCG nuclear export NF-κB CRM1

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CREBBP/EP300 mutations promoted tumor progression in diffuse large B-cell lymphoma through altering tumorassociated macrophage polarization via FBXW7-N0TCHCCL2/ CSF1 axis

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Signal Transduction and Targeted Therapy 2021年第2期6卷 482-495页

作者： Yao-Hui Huang Kun Cai Peng-Peng Xu Li Wang Chuan-Xin Huang Ying Fang Shu Cheng Xiao Jian Sun Feng Liu Jin-Yan Huang Meng-Meng Ji Wei-Li Zhao Shanghai Istitute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiRulin Hospital Afliated to Shanghai Jiao Tong University School of MedicineShanghaiChina School of Life Sciences and Biotechnology.Shanghai Jiao Tong Universiy ShanghalChina Department of Immunobiology and Microbiology Shanghai Istitute of ImmunologyShanghai Jiao Tong University School of MedicineShanghaiChina Pole de Recherches Sino Francais en Science du Vivant et Genomique Laboratory of Molecular PathologyShanghalChina

Epigenetic alterations play an important role in tumor progression of diffuse large B-cell lymphoma(DL BCL).However,the biological relevance of epigenetic gene mutations on tumor microenvironment remains to be *** core set of genes relating to histone methylation(KMT2D,KMT2C,EZH2),histone acetylation(CREBBP,EP300),DNA methylation(TET2),and chromatin remodeling(ARID1A)were detected in the training cohort of 316 patients by whole-genome/exome sequencing(WGS/WES)and in the validation cohort of 303 patients with newly diagnosed DL BCL by targeted *** correlation with peripheral blood immune cells and clinical outcomes were *** mechanisms on tumor microenvironment were investigated both in vitro and in *** all 619 DLBCL patients,somatic mutations in KMT2D(19.5%)were most frequently observed,followed by mutations in ARID1A(8.7%),CREBBP(8.4%),KMT2C(8.2%),TET2(7.8%),EP300(6.8%),and EZH2(2.9%).Among them,CREBBP/EP300 mutations were signifcantly associated with decreased peripheral blood absolute lymphocyte-to-monocyte ratios,as well as inferior progression-free and overall *** B-lymphoma cells,the mutation or knockdown of CREBBP or EP300 inhibited H3K27 acetylation,downregulated FBXW7 expression,activated the NOTCH pathway,and downstream CCL2/CSF1 expression,resulting in tumor-associated macrophage polarization to M2 phenotype and tumor cell *** B-lymphoma murine models,xenografted tumors bearing CREBBP/EP300 mutation presented lower H3K27 acetylation,higher M2 macrophage recruitment,and more rapid tumor growth than those with CREBBP/EP300 wild-type control via FBXW7-NOTCH-CCL2/CSF1 *** work thus contributed to the understanding of aberrant histone acetylation regulation on tumor microenvironment as an alternative mechanism of tumor progression in DLBCL.

关键词： FBXW7 P300 macrophage

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DDB1-and CUL4-associated factor 8 plays a critical role in spermatogenesis

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Frontiers of Medicine 2021年第2期15卷 302-312页

作者： Xiuli Zhang Zhizhou Xia Xingyu Lv Donghe Li Mingzhu Liu Ruihong Zhang Tong Ji Ping Liu Ruibao Ren Shanghai Institute of Hematology State Key Laboratory for Medical GenomicsNational Research Center for Translational Medicine at ShanghaiCollaborative Innovation Center of HematologyRuijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China Key Laboratory of Laparoscopic Technology of Zhejiang Province Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhou 310058China Department of General Surgery Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhou 310058China

Cullin-RING E3 ubiquitin ligase(CRL)-4 is a member of the large CRL family in *** plays important roles in a wide range of cellular processes,organismal development,and physiological and pathological ***1-and CUL4-associated factor 8(DCAF8)is a WD40 repeat-containing protein,which serves as a substrate receptor for *** physiological role of DCAF8 is *** this study,we constructed Dcaf8 knockout *** mice were viable with no noticeable ***,the fertility of Dcaf8-deficient male mice was markedly impaired,consistent with the high expression of DCAF8 in adult mouse *** movement characteristics,including progressive motility,path velocity,progressive velocity,and track speed,were significantly lower in Dcaf8 knockout mice than in wild-type(WT)***,the total motility was similar between WT and Dcaf8 knockout *** than 40%of spermatids in Dcaf8 knockout mice showed pronounced morphological abnormalities with typical bent head *** acrosome and nucleus of Dcaf8 knockout sperm looked similar to those of WT *** vitro tests showed that the fertilization rate of Dcaf8 knockout mice was significantly *** results demonstrated that DCAF8 plays a critical role in spermatogenesis,and DCAF8 is a key component of CRL4 function in the reproductive system.

关键词： Dcaf8 male infertility spermatogenesis

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Palmitoylation of GNAQ/11 is critical for tumor cell proliferation and survival in GNAQ/11-mutant uveal melanoma

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Frontiers of Medicine 2022年第5期16卷 784-798页

作者： Yan Zhang Baoyuan Zhang Yongyun Li Yuting Dai Jiaoyang Li Donghe Li Zhizhou Xia Jianming Zhang Ping Liu Ming Chen Bo Jiao Ruibao Ren Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiCollaborative Innovation Center of HematologyRuijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China Department of Ophthalmology Ninth People’s HospitalShanghai Jiao Tong University School of MedicineShanghai Key Laboratory of Orbital Diseases and Ocular OncologyShanghai 200001China Department of Biology Brandeis UniversityWalthamMA 02454USA

More than 85%of patients with uveal melanoma(UM)carry a GNAQ or GNA11 mutation at a hotspot codon(Q209)that encodes G proteinαsubunit q/11 polypeptides(Gα_(q/11)).GNAQ/11 relies on palmitoylation for membrane association and signal *** the palmitoylation of GNAQ/11 was discovered long before,its implication in UM remains ***,results of palmitoylation-targeted mutagenesis and chemical interference approaches revealed that the loss of GNAQ/11 palmitoylation substantially affected tumor cell proliferation and survival in UM *** inhibition through the mutation of palmitoylation sites suppressed GNAQ/11^(Q209L)-induced malignant transformation in NIH3T3 ***,the palmitoylation-deficient oncogenic GNAQ/11 failed to rescue the cell death initiated by the knock down of endogenous GNAQ/11 oncogenes in UM cells,which are much more dependent on Gα_(q/11) signaling for cell survival and proliferation than other melanoma cells without GNAQ/11 ***,the palmitoylation inhibitor,2-bromopalmitate,also specifically disrupted Gα_(q/11) downstream signaling by interfering with the MAPK pathway and BCL2 survival pathway in GNAQ/11-mutant UM cells and showed a notable synergistic effect when applied in combination with the BCL2 inhibitor,ABT-199,in *** findings validate that GNAQ/11 palmitoylation plays a critical role in UM and may serve as a promising therapeutic target for GNAQ/11-driven UM.

关键词： uveal melanoma mutant GNAQ/11 palmitoylation BCL2 combination target therapy

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DNA crosslinking and recombination-activating genes 1/2(RAG1/2)are required for oncogenic splicing in acute lymphoblastic leukemia

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cancer Communications 2021年第11期41卷 1116-1136页

作者： Hao Zhang Nuo Cheng Zhihui Li Ling Bai Chengli Fang Yuwen Li Weina Zhang Xue Dong Minghao Jiang Yang Liang Sujiang Zhang Jianqing Mi Jiang Zhu Yu Zhang Sai-Juan Chen Yajie Zhao Xiang-Qin Weng Weiguo Hu Zhu Chen Jinyan Huang Guoyu Meng Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational MedicineRui-Jin HospitalSchool of Medicine and School of Life Sciences and BiotechnologyShanghai JiaoTong UniversityShanghai 200025P.R.China Key Laboratory of Synthetic Biology CAS Center for Excellence in Molecular Plant SciencesChinese Academy of SciencesShanghai 200032P.R.China University of Chinese Academy of Sciences Beijing 100049P.R.China Department of Hematologic Oncology State key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhouGuangdong 510060P.R.China Department of Geriatrics Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025P.R.China Medical Center on Aging of Ruijin Hospital Shanghai Jiao Tong University School of MedicineShanghai 200025P.R.China Department of Laboratory Medicine West China HospitalSichuan UniversityChengduSichuan 610044P.R.China Biomedical Big Data Center the First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310000P.R.China cancer Center Zhejiang UniversityHangzhouZhejiang 310000P.R.China

Background:Abnormal alternative splicing is frequently associated with *** B-cell acute lymphoblastic leukemia(B-ALL),double homeobox 4 fused with immunoglobulin heavy chain(DUX4/IGH)can lead to the aberrant production of E-26 transformation-specific family related gene abnormal transcript(ERGalt)and other splicing ***,the molecular mechanism underpinning this process remains ***,we aimed to know how DUX4/IGH triggers abnormal splicing in ***:The differential intron retention analysis was conducted to identify novel DUX4/IGH-driven splicing in B-ALL patients.X-ray crystallography,small angle X-ray scattering(SAXS),and analytical ultracentrifugation were used to investigate how DUX4/IGH recognize double DUX4 responsive element(DRE)-DRE *** ERGalt biogenesis and B-cell differentiation assays were performed to characterize the DUX4/IGH crosslinking *** check whether recombination-activating gene 1/2(RAG1/2)was required for DUX4/IGH-driven splicing,the proximity ligation assay,co-immunoprecipitation,mammalian two hybrid characterizations,in vitro RAG1/2 cleavage,and shRNA knock-down assays were ***:We reported previously unrecognized intron retention events in Ctype lectin domain family 12,member A abnormal transcript(CLEC12Aalt)and chromosome 6 open reading frame 89 abnormal transcript(C6orf89alt),where also harbored repetitive DRE-DRE ***,X-ray crystallography and SAXS characterization revealed that DUX4 homeobox domain(HD)1-HD2 might dimerize into a dumbbell-shape trans configuration to crosslink two adjacent DRE *** DUX4/IGH-mediated crosslinking abolishes ERGalt,CLEC12Aalt,and C6orf89alt biogenesis,resulting in marked alleviation of its inhibitory effect on B-cell ***,we also observed a rare RAG1/2-mediated recombination signal sequence-like DNA edition in DUX4/IGH target ***,shRNA knock-down of RAG1/2 in leukemic Reh cells c

关键词： Acute lymphoblastic leukemia alternative splicing DUX4/IGH ERG_(alt) RAG1/2

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Therapeutic targeting miR130b counteracts diffuse large B-cell lymphoma progression via OX40/OX40L-mediated interaction with Th17 cells

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Signal Transduction and Targeted Therapy 2022年第4期7卷 1297-1310页

作者： Rui Sun Pei-Pei Zhang Xiang-Qin Weng Xiao-Dong Gao Chuan-Xin Huang Li Wang Xiao-Xia Hu Peng-Peng Xu Lin Cheng Lu Jiang Di Fu Bin Qu Yan Zhao Yan Feng Hong-Jing Dou Zhong Zheng Wei-Li Zhao Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiRuijin HospitalShanghai Jiao Tong University of MedicineShanghaiChina State Key Laboratory of Metal Matrix Composites School of Materials Science and EngineeringNational Research Center for Translational Medicine at ShanghaiShanghai Jiao Tong UniversityShanghaiChina Department of Immunobiology and Microbiology Shanghai Institute of ImmunologyShanghai Jiao Tong University School of MedicineShanghaiChina Department of Laboratory Medicine Shanghai RuiJin HospitalShanghai Jiao Tong University School of MedicineShanghaiChina State Key Laboratory of Microbial Metabolism School of Life Sciences and BiotechnologyShanghai Jiao Tong UniversityShanghaiChina

MicroRNAs(miRNAs)are involved in lymphoma progression by regulating the tumor *** miR130b is overexpressed in diffuse large B-cell lymphoma(DLBCL),inducing Th17 cell *** further illustrate its biological significance and therapeutic rationale,miR130b was detected by quantitative real-time PCR in the serum samples of 532 newly diagnosed DLBCL *** mechanism of miR130b on lymphoma progression and the tumor microenvironment was investigated both in vitro and in *** targeting miR130b was also evaluated,including OX40 agonistic antibody and lipid nanoparticles(LNPs)-miR130b *** results showed that serum miR130b significantly correlated with tumor miR130b and serum interleukin-17,indicating lymphoma relapse and inferior survival of DLBCL ***130b overexpression altered tumor microenvironment signaling pathways and increased Th17 cell *** mechanism of action,miR130b downregulated tumor OX40L expression by directly targeting IFNAR1/p-STAT1 axis,recruiting Th17 cells via OX40/OX40L interaction,thereby promoting immunosuppressive function of Th17 *** co-culture systems of B-lymphoma cells with immune cells,miR130b inhibited lymphoma cell autophagy,which could be counteracted by OX40 agonistic antibody and LNPs-miR130b *** murine xenograft model established with subcutaneous injection of A20 cells,both OX40 agonistic antibody and LNPs-miR130b antagomir remarkably inhibited Th17 cells and retarded miR130b-overexpressing tumor *** conclusion,as an oncogenic biomarker of DLBCL,miR130b was related to lymphoma progression through modulating OX40/OX40L-mediated lymphoma cell interaction with Th17 cells,attributing to B-cell lymphoma sensitivity towards OX40 agonistic *** miR130b using LNPs-miR130b antagomir could also be a potential immunotherapeutic strategy in treating OX40-altered lymphoid malignancies.

关键词： lymphoma miR130b inhibited

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The LIFR-targeting small molecules EC330/EC359 are potent ferroptosis inducers

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Genes & Diseases 2023年第3期10卷 735-738页

作者： Chang-Zhou Feng Ning-Zhe Li Xi-Bo Hu Yin-Yin Xie Qiu-Hua Huang Jianming Zhang Zhu Chen Sai-Juan Chen Fudi Wang Xiao-Jian Sun Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiRuijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China School of Life Sciences&Biotechnology Shanghai Jiao Tong UniversityShanghai 200240China The First Affiliated Hospital School of Public HealthInstitute of Translational MedicineZhejiang University School of MedicineHangzhouZhejiang 310058China The First Affiliated Hospital Hengyang Medical SchoolUniversity of South ChinaHengyangHunan 421001China

Ferroptosis is a form of regulated cell death characterized by iron-dependent overaccumulation of lipid peroxides,which causes membrane damage and cell *** can be prevented by cellular antioxidant mechanisms such as glutathione peroxidase 4(GPX4)-mediated elimination of the lipid peroxides at the cost of glutathione(GSH).As the rate-limiting step of GSH synthesis,the availability of intracellular cystine is controlled by the cell membrane-located cystine/glutamate antiporter system xc−.Indeed,the initially identified small molecule inducers of ferroptosis,RSL3 and erastin,turned out to be inhibitors of GPX4 and system xc−,respectively.

关键词： system initially limiting

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Advances in targeted therapy for malignant lymphoma

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Signal Transduction and Targeted Therapy 2020年第1期5卷 2234-2279页

作者： Li Wang Wei Qin Yu-Jia Huo Xiao Li Qing Shi John E.J.Rasko Anne Janin Wei-Li Zhao State Key Laboratory of Medical Genomics Shanghai Institute of HematologyShanghai Rui Jin HospitalShanghai Jiao Tong University School of Medicine197 Rui Jin Er RoadShanghaiChina Pôle de Recherches Sino-Français en Science du Vivant et Génomique Laboratory of Molecular PathologyShanghaiChina Gene&Stem Cell Therapy Program Centenary Institute Sydney Medical SchoolUniversity of SydneyCamperdownAustralia Cell and Molecular Therapies Royal Prince Alfred HospitalCamperdownAustralia U1165 Inserm/UniversitéParis 7 Hôpital Saint LouisParisFrance

The incidence of lymphoma has gradually increased over previous decades,and it ranks among the ten most prevalent cancers *** the development of targeted therapeutic strategies,though a subset of lymphoma patients has become curable,the treatment of refractory and relapsed diseases remains *** efforts have been made to explore new targets and to develop corresponding *** addition to novel antibodies targeting surface antigens and small molecular inhibitors targeting oncogenic signaling pathways and tumor suppressors,immune checkpoint inhibitors and chimeric antigen receptor T-cells have been rapidly developed to target the tumor *** these targeted agents have shown great success in treating lymphoma patients,adverse events should be *** selection of the most suitable candidates,optimal dosage,and effective combinations warrant further *** this review,we systematically outlined the advances in targeted therapy for malignant lymphoma,providing a clinical rationale for mechanism-based lymphoma treatment in the era of precision medicine.

关键词： lymphoma targeted dosage

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