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Aldh2 deficiency plays a dual role in lung tumorigenesis and tumor progression

Genes & Diseases 2024年第3期11卷 144-147页

作者： Hongjia Zhang Xueqian Sun Zhanming Li Tingting Liu Fang Zhang Xinyu Meng Kaimi Li Jianhua Xu Wei He Bo Jing Tong Wang Na Ni Beibei Sun Feng yao yadi Wu Qi Wang Jing Du eugene y.chin Binhua P.Zhou Ping Jiang Lishun Wang Jiong Deng Key Laboratory of Cell Differentiation and Apoptosis of chinese Minister of Education Department of PathophysiologyShanghai Jiao Tong University School of MedicineShanghai 200025China Shanghai Key Laboratory for Tumor Microenvironment and Inflammation Shanghai Jiao Tong University School of MedicineShanghai200025China Department of Pathology Kunming Medical UniversityKunmingYunnan 650500China Medical Research Center Binzhou Medical University HospitalBinzhouShandong 256600China Center for Traditional chinese Medicine and Gut Microbiota Minhang HospitalFudan UniversityShanghai 201100China Department of Radiation Oncology Yantai Affiliated Hospital of Binzhou Medical UniversityYantaiShandong 264100China Department of Pathology Molecular Pathology Research CenterPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Laboratory Medicine Shanghai Pulmonary Hospital Affiliated Tongji UniversityShanghai 200080China Department of Physiology School of Basic Medical SciencesWeifang Medical UniversityWeifangShandong 261021China Department of Thoracic Surgery Shanghai Chest HospitalShanghai Jiao Tong UniversityShanghai 200030China Department of Molecular and Celular Biochemistry Markey Cancer CenterUniversity of Kentucky College of MedicineLexingtonKY40506USA Department of Respiratory Medicine The Second Affiliated HospitalDalian Medical UniversityDalianLiaoning116023China Peninsular Cancer Center Binzhou Medical UniversityYantaiShandong 264003China

Alcohol consumption contributes to global mortality and cancer ***(ACE),the oxidized metabolite of alcohol,is highly reactive towards DNA,resulting in DNA *** can be detoxified to acetate by acetaldehyde dehydrogenase... 详细信息

关键词： mortality damage ALDH2

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Bcl-3 promotes Wnt signaling by maintaining the acetylation ofβ-catenin at lysine 49 in colorectal cancer

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1913-1924页

作者： Xi Chen Chen Wang yuhang Jiang Qi Wang yu Tao Haohao Zhang yongxu Zhao yiming Hu Cuifeng Li Deji ye Dandan Liu Wenxia Jiang eugene y.chin Sheng Chen yongzhong Liu Mingliang Wang Sanhong Liu Xiaoren Zhang CAS Key Laboratory of Tissue Microenvironment and Tumor Shanghai Institute of Nutrition and HealthShanghai Institutes for Biological SciencesUniversity of Chinese Academy of SciencesChinese Academy of SciencesShanghai 200025China Shanghai Institute for Advanced Immunochemical Studies ShanghaiTech UniversityShanghai 201210China Affiliated Cancer Hospital&Institute of Guangzhou Medical University Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and DegradationState Key Laboratory of Respiratory DiseaseGuangzhou 510000China Renji Hospital Shanghai Jiao Tong University School of MedicineShanghai 200025China State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong University School of MedicineShanghai 200032China Department of General Surgery Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Wnt/β-catenin signaling plays a critical role in colorectal cancer(CRC)tumorigenesis and the homeostasis of colorectal cancer stem cells(CSCs),but its molecular mechanism remains unclear.B-cell lymphoma 3(Bcl-3),a member of the IκB family,is overexpressed in CRC and promotes ***,we report a novel function of Bcl-3 in maintaining colorectal CSC homeostasis by activating Wnt/β-catenin *** Bcl-3 suppresses the self-renewal capacity of colorectal CSCs and sensitizes CRC cells to chemotherapeutic drugs through a decrease in Wnt/β-catenin ***,our data show that Bcl-3 is a crucial component of Wnt/β-catenin signaling and is essential forβ-catenin transcriptional activity in CRC ***,Wnt3a increases the level and nuclear translocation of Bcl-3,which binds directly toβ-catenin and enhances the acetylation ofβ-catenin at lysine 49(Ac-K49-β-catenin)and transcriptional ***-3 depletion decreases the Ac-K49-β-catenin level by increasing the level of histone deacetylase 1 to remove acetyl groups fromβ-catenin,thus interrupting Wnt/β-catenin *** CRC clinical specimens,Bcl-3 expression negatively correlates with the overall survival of CRC patients.A significantly positive correlation was found between the expression of Bcl-3 and Ac-K49-β-***,our data reveal that Bcl-3 plays a crucial role in CRC chemoresistance and colorectal CSC maintenance via its modulation of the Ac-K49-β-catenin,which serves as a promising therapeutic target for CRC.

关键词： colorectal homeostasis cancer

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m TOR and post-translational modifications rely on mitochondrion as the arsenal for cellular metabolism regulation

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Science china(Life Sciences) 2015年第8期58卷 810-812页

作者： ZHUGE ChunChun J CHEN Si J chin y eugene Shanghai Chest Hospital Shanghai Jiaotong University Institute of Health Sciences Chinese Academy of Sciences School of Medicine Shanghai Jiaotong University

Mitochondrion is considered as the"powerhouse of the cell"almost immediately since its *** carries less than 1,000 proteins and some nucleotides as well as *** is also discovered as the"lung of the cell"for its role i... 详细信息

关键词：细胞器线粒体翻译后修饰代谢调节 mTOR 呼吸作用代谢过程核苷酸

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肺表面活化蛋白A相似分子在炎症肠道疾病组织中的过量表达(英文)

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中南大学学报（医学版） 2008年第11期33卷 979-986页

作者：罗俊铭刘昭前 chin y.eugene 肾脏研究所堪萨斯大学医学院中南大学临床药理研究所遗传药理学湖南省重点实验室外科学研究室布朗大学医学院

目的:阐明炎症肠道疾病(inlammatory bowel disease,IBD)中肺表面活化蛋白A(pulmonary surfactant protein A,SP-A)相似分子的分布特征和CD68阳性巨噬细胞的免疫反应。方法:外科手术获得的结肠组织标本来自布朗大学医学院罗得岛医院病理... 详细信息

目的:阐明炎症肠道疾病(inlammatory bowel disease,IBD)中肺表面活化蛋白A(pulmonary surfactant protein A,SP-A)相似分子的分布特征和CD68阳性巨噬细胞的免疫反应。方法:外科手术获得的结肠组织标本来自布朗大学医学院罗得岛医院病理科,应用免疫组织化学方法检测IBD患者肠道组织中SP-A相似分子的表达。结果:SP-A相似分子分布在肠道上皮、肠道绒毛表面,连接组织血管和某些炎症细胞。具有SP-A相似分子和CD68阳性表达的巨噬细胞数量炎症区域明显增加,高于正常组织。而免疫荧光双标记实验显示,一些CD68阳性巨噬细胞可以表达SP-A相似分子免疫反应。结论:SP-A是肺脏一种重要的宿主防御因子。

关键词：炎症肠道疾病肺表面活化蛋白A相似分子 CD68 免疫组织化学

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Reversible acetylation modulates dishevelled-2 puncta formation in canonical Wnt signaling activation

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1437-1440页

作者： Jinhong Shen Lin Hu Li yang Mengshi Zhang Weihong Sun Xiaomei Lu Gufa Lin Chao Huang Xiaoren Zhang y.eugene chin CAS Key Laboratory of Tissue Microenvironment and Tumor Institute of Health SciencesShanghai Jiao Tong University School of Medicine&Shanghai Institutes for Biological SciencesChinese Academy of SciencesUniversity of Chinese Academy of Sciences200031 ShanghaiChina Institutes of Biology and Medical Sciences Soochow University Medical College215000 SuzhouJiangsuChina Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education Orthopaedic Department of Tongji HospitalSchool of Life Sciences and TechnologyTongji University200065 ShanghaiChina Clinical Medical Research Institute First Affiliated Hospital of Xinjiang Medical University830054 UrumuqiXinjiangChina

Dear Editor,Dishevelled-2(DVL2)is a central adaptor protein that propagates signals from upstream receptors to downstream effectorβ-catenin in canonical Wnt *** high local concentration,DVL2 assembles into signalosomes through DIX domain-mediated homo-polymerization to provide a docking platform for the recruitment of signaling components,which is critical for Wnt signaling transduction and activation;1 however,the exact underlying mechanism remains *** the roles of phosphorylation and ubiquitination in DVL2-puncta formation have been discussed before,2 the impact of lysine acetylation of DVL2 on this process remains *** we investigated the effect of acetylation on DVL2-puncta formation.

关键词： activation canonical upstream

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原位杂交研究GPRC6AmRNA在小鼠组织中的分布规律

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中南大学学报（医学版） 2010年第1期35卷 1-10页

作者：罗俊铭刘昭前刘景诗 chin y.eugene 堪萨斯大学医学院肾脏研究所美国堪萨斯66160 中南大学湘雅二医院病理科长沙410011 中南大学临床药理研究所遗传药理学湖南省重点实验室长沙410078 湖南师范大学第一附属医院麻醉科长沙410004 布朗大学医学院外科学研究室美国罗得岛02903

目的:探讨G蛋白偶联受体C组6A(Gprotein-coupled receptor family C,group6,subtype A,GPRC6A)mRNA在小鼠体内的分布规律。方法:比较传统和TSA信号放大系统分析石蜡包埋的小鼠组织中GPRC6A mRNA的分布情况。为了确保信号特异性,将GPRC6... 详细信息

目的:探讨G蛋白偶联受体C组6A(Gprotein-coupled receptor family C,group6,subtype A,GPRC6A)mRNA在小鼠体内的分布规律。方法:比较传统和TSA信号放大系统分析石蜡包埋的小鼠组织中GPRC6A mRNA的分布情况。为了确保信号特异性,将GPRC6A基因剔除小鼠组织放在同一张切片上作阴性对照。结果:建立了一种用非同位素标记的互补RNA探针原位杂交检测石蜡包埋的小鼠组织中低表达GPRC6A mRNA的方法。TSA信号放大系统明显提高原位杂交检测该受体的敏感性。GPRC6A基因剔除小鼠组织中没有可测信号。GPRC6A mRNA至少在消化腺、副消化腺中表达,同时也在肾、睾丸、子宫、脑、肌肉脂肪中有表达。结论:GPRC6A mRNA的分布模式与GPRC6A基因剔除小鼠的基因表型基本一致。

关键词： GPRC6A mRNA 小鼠分布模式 TSA信号放大系统原位杂交

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Skeletal myoblast based delivery of angiogenic growth factors:a comparison between angiopoietin-1 and VEGF gene delivery for therapeutic angiogenesis in the heart

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Journal of Geriatric Cardiology 2006年第3期3卷 152-160页

作者： Husnain Kh Haider In-chin Song Peter K Law eugene KW Sim Department of Pathology and Laboratory Medicine University of Cincinnati Ohio United States Departmet of Experimental Surgery Singapore General Hospital Singapore Cell Transplants Singapore Pte Ltd Singapore Department of Surgery National University of Singapore Singapore & Gleneagles JPMC Cardiac Center Brunei Darussalam Singapore

Objectives This study investigated the efficacy of human skeletal myoblasts (SkM) mediated either human vascular endothelial growth factor-165 (hVEGF165) or angiopoietin-1 (Ang-1) on vascular development and myocardial regional perfusion. Methods A porcine heart model of chronic infarction was created in 28 female swine by coronary artery ligation. The animals were randomized into: (1) group-1, DMEM injected (n=6), (2) group-2, Ad-null transduced SkM transplanted (n=6), (3) group-3, Ad-hVEGF165 transduced SkM transplanted (n=8), and (4) group-4, Ad-Ang-1 transduced SkM (n=8). Three weeks later, 5 ml DMEM containing 3×108 SkM carrying exogenous genes were intramyocardially injected into 20 sites in left ventricle in groups-2, -3 and -4. Animals in group-1 were injected 5 ml DMEM without cells. Animals were kept on 5 mg/kg cyclosporine per day for 6 weeks. Regional blood flow was measured using fluorescent microspheres. The heart was explanted at 2, 6 and 12 weeks after transplantation for histological studies. Results Histological examination showed survival of lac-z expressing myoblasts in host tissue. Capillary density based on Von Willebrand factor-VIII (vWF-VIII) at low power field (×100) was 57.13±11.85 in group-3 at 6 weeks and declined to 32.1±5.21 at 12 weeks, while it was 39.9±10.26 at 6 weeks and increased to 45.14±6.54 at 12 weeks in group-4. The mature blood vessel index was highest in group- 4 at 6 and 12 weeks after transplantation. The regional blood flow in the center and peri-infarct area was significantly increased in animals of groups-3 and -4. Conclusions SkM carrying either hVEGF165 or Ang-1 induced neovascularization with increased blood flow. Ang-1 overexpression resulted in mature and stable blood vessel formation and may be a more potent arteriogenic inducer for neovascularization.

关键词： therapeutic angiogenesis skeletal myoblasts vascular endothelial growth factor-165 angiopoietin-1 myocardial infarction

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SENP1 regulates IFN-γ-STAT1 signaling throug STAT3-SOCS3 negative feedback loop

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Journal of Molecular Cell Biology 2017年第2期9卷 144-153页

作者： Tingting yu yong Zuo Rong Cai Xian Huang Shuai Wu Chenxi Zhang y. eugene chin Dongdong Li Zhenning Zhang Nansong Xia Qi Wang Hao Shen Xuebiao yao Zhong-yin Zhang Song Xue Lei Shen Jinke Cheng Department of Biochemistry and Molecular Cell Biology Shanghai Key Laboratory for Tumor Microenvironment and Inflammation Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Key Laboratory of Cell Differentiation and Apoptosis of chinese Ministry of Education Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Department of Developmental Genetics School of Basic Medical Sciences Nanjing Medical University Nanjing 211166 China Shanghai Institute of Immunology Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Institute of Health Sciences Chinese Academy of Sciences Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Department of Microbiology University of Pennsylvania Perelman School of Medicine Philadelphia PA 19104 USA Anhui Key Laboratory of Cellular Dynamics Hefei National Laboratory for Physical Sciences at Nanoscale University of Science and Technology of ChinaHefei 230026 China Department of Biochemistry and Molecular Biology Indiana University School of Medicine Indianapolis IN 46202 USA Shanghai Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200127 China

Interferon-γ （IFN-γ） triggers macrophage for inflammation response by activating the intracellular JAK-STAT1 signaling. Suppressor of cytokine signaling 1 （SOCS1） and protein tyrosine phosphatases can negatively modulate IFN-γ signaling. Here, we identify a novel negative feedback loop mediated by STAT3-SOCS3, which is tightly controlled by SENP1 via de-SUMOylation of protein tyrosine phosphatase 1B （PTPIB）, in IFN-y signaling. SENP1-deficient macrophages show defects in IFN-γ signaling and M1 macrophage activation. PTP1B in SENP1-deficient macrophages is highly SUMOylated, which reduces PTP1B-induced de-phosphorylation of STAT3. Activated STAT3 then suppresses STAT1 activation via SOCS3 induction in SENP1-deficient macro- phages. Accordingly, SENP1-deficient macrophages show reduced ability to resist Listerio rnonocytogenes infection. These results reveal a crucial role of SENP1-controlled STAT1 and STAT3 balance in rnacrophage polarization.

关键词： IFN-γ macrophage SENP1 SUMOylation

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Human myoblast genome therapy

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Journal of Geriatric Cardiology 2006年第3期3卷 135-151页

作者： Peter K Law Danlin M Law eugene KW Sim Khawja H Haider Margarita N Vakhromeeva Ilia I Berishvili Leo A Bockeria Choong-chin Liew Cell Transplants Asia Ltd. Canada National University Medical Institutes National University of Singapore Singapore Department of Pathology and Laboratory Medicine University of Cincinnati Ohio USA Bakoulev Scientific Center for Cardiovascular Surgery Russian Academy of Medical Sciences Russia Bingham and Women's Hospital The Cardiovascular Genome Unit Harvard Medical School USA

Human Myoblast Genome Therapy (HMGT) is a platform technology of cell transplantation, nuclear transfer, and tissue engineering. Unlike stem cells, myoblasts are differentiated, immature cells destined to become muscles. Myoblasts cultured from satellite cells of adult muscle biopsies survive, develop, and function to revitalize degenerative muscles upon transplantation. Injection injury activates regeneration of host myofibers that fuse with the engrafted myoblasts, sharing their nuclei in a common gene pool of the syncytium. Thus, through nuclear transfer and complementation, the normal human genome can be transferred into muscles of patients with genetic disorders to achieve phenotype repair or disease prevention. Myoblasts are safe and efficient gene transfer vehicles endogenous to muscles that constitute 50% of body weight. Results of over 280 HMGT procedures on Duchenne Muscular Dystrophy (DMD) subjects in the past 15 years demonstrated absolute safety. Myoblast-injected DMD muscles showed improved histology. Strength increase at 18 months post-operatively averaged 123%. In another application of HMGT on ischemic cardiomyopathy, the first human myoblast transfer into porcine myocardium revealed that it was safe and effective. Clinical trials on approximately 220 severe cardiomyopathy patients in 15 countries showed a y. Most subjects received autologous cells implanted on the epicardial surface during coronory artery bypass graft, or injected on the endomyocardial surface percutaneously through guiding catheters. Significant increases in left ventricular ejection fraction, wall thickness, and wall motion have been reported, with reduction in perfusion defective areas, angina, and shortness of breath. As a new modality of treatment for disease in the skeletal muscle or myocardium, HMGT emerged as safe and effective. Large randomized multi-center trials are under way to confirm these preliminary results. The future of HMGT is bright and exciting.

关键词： heart regeneration human genome therapy myoblasts

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β-arrestin在肾间质纤维化中的作用及机制

β-arrestin在肾间质纤维化中的作用及机制

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中国生理学会肾脏生理专业委员会第二届学术年会

作者：赵莉芹王艳道 y.eugene chin 余晨同济大学附属同济医院肾脏科中国科学院健康所

目的:肾素—血管紧张素系统(RAS)过度激活是促进肾脏纤维化的关键之一,长期肾间质纤维化最终发展成肾功能衰竭。近年对RAS认识有重要突破:当血管紧张素II(AngII)激活1型受体(ATlR)后,其下游信号通路除了传统认识的G蛋白偶联通路,还有一...

目的:肾素—血管紧张素系统(RAS)过度激活是促进肾脏纤维化的关键之一,长期肾间质纤维化最终发展成肾功能衰竭。近年对RAS认识有重要突破:当血管紧张素II(AngII)激活1型受体(ATlR)后,其下游信号通路除了传统认识的G蛋白偶联通路,还有一条新认识的β-arrestin依赖性信号通路,两条通路各自独立,具有不同生物学效应。

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