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Role of apoptosis resistance in immune evasion and metastasis of colorectal cancer

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World Journal of gastrointestinal Oncology 2010年第11期2卷 399-406页

作者： Kebin Liu, Department of Biochemistry and molecular Biology, medical college of georgia, {2. Health Sciences University, augusta, ga 30912, United States Kebin Liu Department of Biochemistry and Molecular Biology Medical College of Georgia Georgia Health Sciences University Augusta GA 30912 United States.

The host immune system functions as a guardian against tumor development. It has been demonstrated that cytotoxic T lymphocyte (CTL)-mediated cytotoxic pathways function to inhibit or delay human colorectal cancer development. However, the host anti-tumor immune responses also 'edit' the tumor and select for more aggressive variants, resulting in immune evasion and tumor escape. Fas is a death receptor that mediates one of the major cytotoxic effector mechanisms of the CTLs. Fas is highly expressed in normal human colon epithelial cells but is frequently silenced in colorectal carcinoma, especially in metastatic colorectal carcinoma, suggesting that loss of Fas expression and function may be an immune evasion and tumor escape mechanism. In addition, recent studies indicated that Fas also mediates cellular proliferation signaling pathways to promote tumor development. Therefore, the death receptor Fas may not only transduce death signals to suppress tumor development but also activate cellular proliferation and the migration process to promote tumor growth and progression. Thus, understanding the mechanisms by which the Fas receptor and its associated protein complex transduces the death and survival signals may identify molecular targets for the development of therapeutic strategy to enhance the Fas-mediated death signals to increase the efficacy of cancer immunotherapy.

关键词： Apoptosis Fas Metastasis Immune evasion

Neuregulin and schizophrenia

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Neuregulin and schizophrenia

molecular structure and biological function of proliferating cell nuclear antigen

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Lin MEI institute of molecular {2. and genetics and Department of Neurology,medical college of georgia,augusta, georgia 30912,usa

＜正＞Neuregulin 1（NRG1） is a large family of EGF domain-containing trophic factors that are widely expressed in the *** acts by stimulating ErbB receptor tyrosine kinases including ***1 signaling has been implicated in various steps of neural development including neuron migration,neurite outgrowth,synapse formation,and *** NRG1 and ErbB4 are susceptibility genes of schizophrenia and their expression and activity appear abnormal in the brain of schizophrenic patients although involved pathologic mechanisms are poorly *** light of high expression of ErbB4 in parvalbumin（PV）-immunoreactive interneruons,we have studied its role in synapse formation and synaptic plasticity of PV-positive intemeurons by using a combination of in vitro and in vivo techniques.I will report and discuss recent data that support the following working ***,during development,NRG1 appears to promote the formation of excitatory synapses in PV-positive intemeuons,probably by stabilizing *** effect requires the tyrosine kinase activity of ***,both NRG1 and ErbB4 are expressed in adult ***1 was able to stimulate gaBA release from PV-positive intemeurons and thus reduces the firing of pyramidal *** suggests that acute suppression of the induction of long-term potentiationby NRG1 requires ErbB4 in PV-positive ***,mutant mice where the ErbB4 gene is specifically ablated in PV-positive neurons exhibit schizophrenia-related phenotypes including hyperactivity,reduced prepulse inhibition and impaired working *** results highlight a role of NRG1/ErbB4 signaling in PV-positive interneurons in forming gaBAergic circuitry and regulating its function and suggest that PV-positive intemeurons may be a cellular target of NRG1 signaling in complex behaviors relevant to *** findings contribute to a better understanding of how abnormal NRG1/ErbB4 signaling may contribute to schizophrenia pathogenesis

关键词： schizophrenia neuregulin ErbB4 interneurons gaBA candidate genes neural development plasticity

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Progress in Natural Science:Materials International 2007年第10期17卷 1127-1135页

作者： Song Nanmeng1, Sang Jianli1 and Xu Heng2.1. institute of Cell Biology, college of Life Science, Beijing Normal University, Beijing 100875, China 2. Emory University School of {2., ga 30332. usa) institute of Cell Biology College of Life Science Beijing Normal University Beijing 100875 China School of medicine Emory University GA 30332 United States

Proliferating cell nuclear antigen (PCNA) is the core component of replication complex in eukaryote. As a processive factor of DNA polymerase delta, PCNA coordinates the replication process by interacting with various replication proteins. PCNA appears to play an essential role in many cell events, such as DNA damage repair, cell cycle regulation, and apoptosis, through the coordination or organization of different partners. PCNA is an essential factor in cell proliferation, and has clinical significance in tumor research. In this article we review the functional structure of PCNA, which acts as a function switch in different cell events.

关键词： PCNA Function Switch PCNA Binding Motif Cell Cycle DNA Replication DNA Repair.

Intramuscular delivery of rAAV-mediated kallikrein gene reduces hypertension and prevents cardiovascular injuries in model rats

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Acta Pharmacologica Sinica 2007年第12期28卷 1898-1906页

作者： Yao WANG~(2.3),Ling-bo HOU~(2.3),Zhen-jun LIU~2.Yan WANG~2.Chun-lian CHEN~2.Xiao XIAO~(2.4),Dao-wen WANG~(2.5)~2.institute of Hypertension and Department of Internal medicine,Tongji Hospital,Tongji {2. college,Huazhong University of Science andTechnology,Wuhan 430030,China ~4 Departments of molecular genetics and Biochentistry and Gene Therapy Center University of Pittsburgh,Pittsburgh,PA 152.1,usa institute of Hypertension and Department of Internal medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Departments of molecular genetics and Biochemistry and Gene Therapy Center University of Pittsburgh Pittsburgh USA

Aim:The overexpression of the human tissue kallikrein （HK） gene can reduceblood pressure and ameliorate the secondary syndromes associated with hyper-tension in animal *** current study was designed to investigate hy-potensive effect of intramuscular delivery of HK ***:We generatedan recombinant adeno-associated virus （rAAV） vector expressing human tissuekallikrein under the control of a cytomegalovirus promoter and administered therAAV-HK vector to a spontaneously hypertensive rat model at a dose of 1×1010virons/rat through intramuscular ***:A persistent,high-level ex-pression of HK post-gene delivery was confirmed by *** systolic bloodpressure in the rats receiving rAAV-LacZ and saline increased from 171.3 mmHg to182.3 mmHg 2. weeks' post *** contrast,the delivery of the HK gene byAAV vectors attenuated the increase of the systolic blood pressure in the *** systolic blood pressure was only slightly lowered （from a level of 174mmHg to 170.5 mmHg） post-vector *** difference in blood pres-sure between the treated group and the control groups is statistically significantat 12.6 *** hypotensive effect of rAAV-HK persisted until the end of thetesting *** addition,a significant amelioration of cardiovascularhypertrophy,renal injury,and collagen depositions in the rAAV-HK-treated ani-mals were also ***:All the effects are comparable with thoseof intravenous ***,the intramuscular administration of rAAV-HKmay be used in gene therapy for hypertension.

关键词： recombinant adeno-associated virus vector human tissue kallikrein intramuscular administration hypertension gene therapy cardiovascular remodeling spontaneously hypertensive rat

Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line

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Cell Research 2006年第4期16卷 356-366页

作者： Xiao Xia Wang~(1,2. Rong Liu~1 Shun Qian Jin~1 Fei Yue Fan~2.Qi Min Zhan~1 ~1State Key Laboratory of molecular Oncology,Cancer institute,Chinese Academy of {2. Sciences and Peking Union {2. college,Beijing 10002.,China ~2.1} of Radiation medicine,Chinese Academy of {2. Sciences and Peking Union {2. college,Tianjin 300192.China State Key Laboratory of molecular Oncology Cancer Institute Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China institute of Radiation medicine Chinese Academy of Medical Sciences and Peking Union Medical College Tianjin China

Aurora-A kinase,a serine/threonine protein kinase,is a potential *** and overexpression of Au-rora-A have been found in several types of human tumors,including esophageal squamous cell carcinoma(ESCC).It hasbeen demonstrated that cells overexpressing Aurora-A are more resistant to cisplatin-induced ***,themolecular mechanisms mediating these effects remain largely *** this report,we showed that overexpressionof Aurora-A through stable transfection of pEGFP-Aurora-A in human ESCC KYSE150 cells significantly promotedcell proliferation and inhibited cisplatin- or UV irradiation-induced *** of caspase-3 and poly(ADP-ribose)polymerase(PARP)in Aurora-A overexpressing cells were substantially reduced after cisplatin or UV ***,we found that silencing of endogenous Aurora-A kinase with siRNA substantially enhanced sensitivityto cisplatin- or UV-induced apoptosis in human ESCC EC9706 *** parallel,overexpression of Aurora-A potentlyupregulated the expression of ***,the knockdown of Bc1-2.by siRNA abrogated the Aurora-A's effect oninhibiting *** together,these data provide evidence that Aurora-A overexpression promoting cell proliferationand inhibiting apoptosis,suggesting a novel mechanism that is closely related to malignant phenotype and anti-cancerdrugs resistance of ESCC cells.

关键词： Aurora-A apoptosis caspase-3 PARP esophageal squamous cell carcinoma (ESCC) siRNA

In vitro reassembly of nuclear envelopes and organelles in Xenopus egg extracts

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Cell Research 2006年第7期16卷 632-640页

作者： Ping Lu~1 Hui Zheng~2.Zhonghe Zhai ~1college of Life Sciences ~2.1} of {2. medicine,Peking University Beijing 100871,China college of Life Sciences Peking University Beijing China institute of molecular {2. Peking University Beijing China

We reconstituted bilayer nuclear membranes,multilayer membranes,and organelles from mixtures of Xenopus laevis eggextracts and demembranated Xenopus sperm *** proportions of the cytosolic and vesicular fractions from theeggs were used in the reconstitution mixtures.A cytosol:vesicle ratio of 10:1 promoted reassembly of the normal bilayernuclear membrane with inserted nuclear pore complexes around the decondensed Xenopus sperm chromatin.A cytosol:vesicle ratio of 5:1 caused decondensed and dispersed sperm chromatin to be either surrounded by or divided by unusualmultilayer membrane structures with inlaid pore complexes.A cytosol:vesicle ratio of 2.5:1 promoted reconstitution ofmitochondria,endoplasmic reticulum networks,and Golgi *** reassembly of the endoplasmic reticulumand Golgi apparatus,vesicular fragments of the corresponding organelles fused together and changed their shape to formflattened cisternae,which were then stacked one on top of another.

关键词： cell-free system endoplasmic reticulum Golgi apparatus mitochondria nuclear reconstitution Xenopus egg extracts

Efflux of potassium ion is an important reason of HL-60 cells apoptosis induced by tachyplesin

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Acta Pharmacologica Sinica 2006年第10期27卷 1367-1374页

作者： Hal-tao ZHANG~(2.4) Jun WU~3 Hai-feng ZHANG~2.Qi-feng ZHU ~2.0} of Biochemistry.and molecular Biology,Guangdong {2. college,Zhanjiang 52.02.,China ~3Affiliated Hospital of Guangdong {2. college,Zhanjiang 52.02.,China institute of Biochemistry and molecular Biology Guangdong Medical College Zhanjiang China Affiliated Hospital of Guangdong medical college Zhanjiang China

Aim:To investigate the role of intercellular potassium in tachyplesin-induced HL-60cells ***:The concentration of intercellular potassium,cell vol-ume and mitochondrial membrane potential were examined by flow ***:The concentration of intercellular potassium reduced in a time-depen-dent manner in tachyplesin-treated HL-60 *** addition,the loss of mitochon-drial membrane potential was tightly coupled with the shrinkage of cell *** caspase inhibitors protected against DNA degradation but did not pre-vent the loss of HL-60 cell viability induced by ***2.,which was akind of blocker of volume-regulatory K+channels,increased the viability oftachyplesin-treated HL-60 cells and maintained mitochondrial membrane potentialand cell ***:Efflux of K+was an important reason for apoptosisin tachyplesin-treated HL-60 *** of K+affected the viability of tachyplesin-treated HL-60 cells independent of the process of caspase activation.

关键词： horseshoe crab tachyplesin intracellular potassium mitochondrial membrane potential HL-60 cell

Effects of Raloxifene on Caveolin-1 mRNA and Protein Expressions in Vascular Smooth Muscle Cells

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Acta Biochimica et Biophysica Sinica 2006年第11期38卷 747-752页

作者： Fa-Lin YANG~(1#*) Hong HE~(2.) Xian-Xi LIU~1* Bing TU~1 Xian-Wei ZENG~3 Ji-Xin SU~1 Xin WANG~2.Qin HU~2. 1 institute of Biochemistry and molecular Biology,{2. college,Shandong University,Jinan 2.0012.China 2.Department of Cardiology,Qilu Hospital,Shandong University,Jinan 2.0012.China 3 Department of Clinical medicine,Weifang {2. college,Weifang 2.0041,China institute of Biochemistry and molecular Biology Medical College Shandong UniversityJinan 250012 China Department of Cardiology Qilu Hospital Shandong UniversityJinan 250012 China Department of Clinical medicine Weifang Medical CollegeWeifang 260041 China

Caveolin-1 is regulated by estrogen in vascular smooth muscle ***,a selectiveestrogen receptor modulator that possibly has cardioprotective properties without an increased risk of canceror other side effects of estrogen,may be used in women with risk of coronary artery ***,therelationship between raloxifene and caveolin-1 is still ***,this study was designed to seewhether raloxifene regulates caveolin-1 expression and if so,whether such regulation is mediated by *** aortic smooth muscle cells were cultured in the absence or presence of raloxifene (10-8to10-6M) for 12.or 2. *** mRNA and protein levels of caveolin-1 were increased significantly after 2. htreatment with *** increases were inhibited by estrogen receptor antagonist ICI 182.80 (10-5M).Results of this study suggest that raloxifene stimulates caveolin-1 transcription and translation throughestrogen receptor mediated mechanisms.

关键词： raloxifene caveolin-1 estrogen receptor vascular smooth muscle cell

Recombinant Neural Protein PrP Can Bind with Both Recombinant and Native Apolipoprotein E In Vitro

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Acta Biochimica et Biophysica Sinica 2006年第9期38卷 593-601页

作者： Chen gaO~1 Yan-Jun LEI~(1,2. Jun HAN~1 Qi SHI~1 Lan CHEN~(1,3) Yan GUO~(1,4) Yong-Jun gaO~1 Jian-Ming CHEN~1 Hui-Ying JIANG~1 Wei ZHOU~1 Xiao-Ping DONG~1* 1 State Key Laboratory for Infectious Disease Prevention and Control,National institute for Viral Disease Control and Prevention,Chinese Center for Disease Control and Prevention,Beijing 100052.China 2.School of medicine,Xi'an Jiaotong University,Xi'an 710061,China 3 National Laboratory of {2. molecular Biology,institute of Basic {2. Science,Chinese Academy of {2. Sciences and Peking Union {2. college,Beijing 100005,China 4 college of Science and Veterinary medicine,Northwest Agriculture and Forest University,Yangling 712.00,China State Key Laboratory for Infectious Disease Prevention and Control National Institute for Viral Disease Control and Prevention Chinese Center for Disease Control and PreventionBeijing 100052 China School of medicine Xi'an Jiaotong UniversityXi'an 710061 China National Laboratory of medical molecular Biology Institute of Basic Medical Science Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100005 China college of Science and Veterinary medicine Northwest Agriculture and Forest UniversityYangling 712100 China

The most essential and crucial step during the pathogenesis of transmissible spongiformencephalopathy is the conformational change of cellular prion protein （PrPC） to pathologic isoform (PrPSc).Alot of data revealed that caveolae-like domains （CLDs） in the cell surface were the probable place where theconversion of PrP proteins *** E （ApoE） is an apolipoprotein which is considered toplay an important role in the development of Alzheimer's disease and other neurodegenerative diseases byforming protein complex through binding to the receptor located in the clathrin-coated pits of the cell *** this study,a 914-bp cDNA sequence encoding human ApoE3 was amplified from neuroblastoma cell *** human ApoE isomers were expressed and purified from Escherichia ***-specificantiserum was prepared by immunizing rabbits with the purified ***/His pull-down assay,immunoprecipitation and ELISA revealed that three full-length ApoE isomers interact with the recombinantfull-length PrP protein in *** regions corresponding to protein binding were mapped in the N-terminalsegment of ApoE （amino acid 1-194） and the N-terminal of PrP （amino acid 2.-90）.Moreover,the recombinantPrP showed the ability to form a complex with the native ApoE from liver *** data provided directevidence of molecular interaction between ApoE and *** also supplied scientific clues for assessing thesignificance of CLDs on the surface of cellular membrane in the process of conformational conversion fromPrPCto PrPScand probing into the pathogenesis of transmissible spongiform encephalopathy.

关键词： prion disease PrP apolipoprotein E protein interaction caveolae-like domain