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检索条件"任意字段=中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议"

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The JNK signaling pathway mediates chrysotile asbestos-inducedalveolar epithelial cell apoptosis

The JNK signaling pathway mediates chrysotile asbestos-induc...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者： Gang Liu Ziying Lin Yahong Wang Jinfeng Tang Haili Huang 广东医学院附属医院临床医学研究中心

Chrysotile asbestos exposure is associated with excess mortality from pulmonary diseasessuch as lung cancer, mesothelioma, and asbestosis. Although multiple mechanisms bywhich chrysotile asbestos fibers induce pulmonary disease have been identified, the roleof apoptosis in human lung alveolar epithelial cells(AEC) has not been fully explored. Accumulatingevidence implicate AEC apoptosis as a crucial event in the development ofidiopathic pulmonary fibrosis(IPF) as well as asbestosis. The goal of this study was to determinewhether chrysotile asbestos induces mitochondria-regulated(intrinsic) AEC apoptosisand, if so, whether this occurs via activation of mitogen-activated protein kinases(MAPK). Using human A549 bronchoalveolar carcinoma-derived cells with alveolar epithelialtype II-like features, we show that chrysotile asbestos induces a dose/timedependentdecrease in cell viability, which is accompanied by the activation of the MAPKc-Jun N-terminal kinases(JNK), but not the MAPKs extracellular signal-regulated kinase(ERK)1/2 and p38. Chrysotile asbestos induces intrinsic AEC apoptosis as evidenced by theup-regulation of pro-apoptotic Bax and Bak along with activation of caspase-9, poly(ADPribose)polymerase(PARP), and cytochrome c release. Notably, SP600125, a specific JNKinhibitor, blocked chrysotile asbestos-induced JNK activation and apoptosis as assessed byboth caspase-9 cleavage and PARP activation. Our results demonstrate that chrysotile asbestosinduces intrinsic AEC apoptosis by a JNK-dependent mechanism and suggests apotential novel target for modulating chrysotile asbestos-related lung diseases.

关键词： chrysotile asbestos apoptosis c-Jun N-terminal kinases(JNK) mitochondriald ysfunction

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Agrobacterium mediated transformation method for transient geneexpression analysis in cotton cotyledon

Agrobacterium mediated transformation method for transient g...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者： Peng He Lei Wang Jianing Yu College of Life Sciences Shaanxi Normal University

In recent years,a large number of uncharacterized novel genes have been identificationaccompanied by the cotton genome large-scale *** investigate the function ofthese unknown genes,usually genetic transformation method is *** cultural transgeniccotton is time-consuming,laboursome and low transformation *** transient gene expression has significantly advantages for quickly andconveniently analyzing gene function compared to traditional genetic *** crops have established transient transformation system for rapid research *** cotton transient transformation system still absent and immaturity,this inhibitedresearch for cotton gene *** this research,we present a novel cotton cotyledon transient expression system by usingGUS expression vector and Agrobacterium tumefacien mediated *** investigatedand analyzed agrobacterium strain,agrobacterium concentration,cotyledon growth time,injection volume of transformation liquid and co-culture *** results showed that(1)Cultured 6 days cotton cotyledons injected 50μl Agrobacterium tumefacien with OD600equal to 0.5,then co-incubated with living cotyledons for 2-3 d,exogenous gene displayedthe highest expression efficiency.(2)Cotton cotyledon is more suitable for establishingtransient expression system than using euphylla to do.(3)Agrobacterium tumefacienLBA4404mediated transient transformation prefers to use *** cotton cotyledontransient expression system,we just need8-12d to getting results from seedling germinationto *** the new method is easy and convenient to manipulate,which provides great value to research promoter activity,protein-protein interaction,subcellular localization for novel genes coming from *** addition,cotton cotyledon transient expression system provides a rapid,efficient andeconomical method to analyze gene function in intact plants with minimal manual handlingand without dedicated d

关键词： cotton transient transformation

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NAMPT Inhibitor FK866 as a Potent Molecule to Promote Drug Sensitivity to Temozolomide in Glioma Cells

NAMPT Inhibitor FK866 as a Potent Molecule to Promote Drug S...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者：王培银李明眏周文科金保哲张晨光江涛张新中丁卫 Department of Neurosurgery The First Affiliated Hospital of Xinxiang Medical University Xinxiang Medical University Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Department of Medical Genetics Cancer Institute Capital Medical University Beijing Institute of Brain Disorders

Glioma is a primary brain tumor with most prevalence and poor prognosis. Temozolomide(TMZ) is the firstline chemotherapy drug to treat glioma patients post ***, the failure of chemotherapy is often seen due to the development of tumorcell resistance to the cytotoxic effects of TMZ. Clinical studies indicated that elevated expressionand low promoter methylation of the repair protein O6-methylguanine-DNAmethyltransferase(MGMT) associated with TMZ resistance. Recently, FK866 was reportedto play important roles in tumorigenesis, metastasis and chemosesitivity in several cancertypes, as a potent inhibitor of NAMPT(Nicotinamide phosphoribosyl transferase, the ratelimitingenzyme of salvage synthesis of NAD). In the present study, we found that patientswith low NAMPT expression manifested a good prognosis independent of the levels ofMGMT promoter methylation, based on the expression microarray data of 220 gliomasamples of all grades from the Chinese Glioma Genome Atlas(CGGA). We further investigatedwhether FK866 was able to affect TMZ sensitivity in U87 human glioma cells. The resultsshowed that a low single dose of 20 nM FK866 significantly increased TMZ-inducedcell death. The IC50 of TMZ was decreased from 350μM to 200μM with the cotreatment of FK866. Meanwhile, increased level of cleaved PARP was observed. As FK866 is being trialedfor lung cancer treatment, our findings suggested its potenial application as a facilitatingagent for glioma chemotherapy, especially for TMZ resistant cases.

关键词： FK866 NAMPT Glioma TMZ Chemotherapy

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Steroid receptor coactivator 1 promotes liver cancer progressionby enhancing cell proliferation and invasion

Steroid receptor coactivator 1 promotes liver cancer progres...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者：童章炜李明王薇莫萍丽刘坤李文岗俞春东厦门大学生命科学学院厦门大学附属成功医院(解放军174医院)

SRC-1 works as a transcriptional coactivator not only for steroid receptors such as androgenreceptor(AR) and estrogen receptor(ER), but also for other transcription factors, suchas PEA3, Ets-2, and AP-1. It has been shown that SRC-1 plays an important role in the progressionof breast cancer and prostate cancer. However, its role in liver cancer progressionremains unknown. In this study, we reported that SRC-1 was upregulated in 24(60%) of 40 human hepatocellular carcinoma(HCC) specimens. Downregulation of SRC-1 decreasedliver cancer cell proliferation, cell invasion, and oncogenic potential in vitro and in *** of SRC-1 resulted in reduced expression of oncogene c-Myc, proliferationmarker proliferating cell nuclear antigen(PCNA), and MMP-9, which has been proven topromote cell invasion and metastasis. Consistent with in vitro results, expression of SRC-1was positively correlated with PCNA and MMP-9 in human HCC specimens, and the expressionlevels of c-Myc in SRC-1-positive HCC specimens were higher than that in SRC-1-negative HCC specimens. In addition, SRC-1 and SRC-3 were co-overexpressed in 45% ofHCC specimens and cooperated to promote HCC cell proliferation. Simultaneous downregulationof SRC-1 and SRC-3 dramatically inhibited HCC cell proliferation. Conclusion:our results demonstrate that SRC-1 is an important regulator of liver cancer progression,and offer a potential of the rapeutic molecular target for liver cancer.

关键词： Steroid receptor coactivator 1 Liver cancer Hepatocellular carcinoma Cellp roliferation Cell invasion

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Depletion of poly(A)-specific ribonuclease(PARN) arrests the cellcycle of human gastric cancer cells in a p53/p21-dependent pathway

Depletion of poly(A)-specific ribonuclease(PARN) arrests the...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者：张丽娜闫永彬清华大学

Regulation of mRNA decay plays a crucial role in the post-transcription control of cellgrowth, survival, differentiation, death and senescence. Deadenylation is a rate-limitingstep in the silence and degradation the bulk of highly regulated mRNAs. However, thephysiological functions of various deadenylases have not been fully deciphered. In this research,we found that poly(A)-specific ribonuclease(PARN) was up-regulated in gastric tumortissues and gastric cancer cell lines MKN28 and AGS. The cellular function of PARNwas investigated by knocking down the endogenous PARN in the MKN28 and AGS *** results showed that PARN-depletion significantly inhibited the proliferation of the twotypes of gastric cancer cells and promoted cell death, but did not significantly affect cellmotility and invasion. The depletion of PARN arrested the gastric cancer cells at the G0/G1 phase by up-regulating the expression levels of p53 and p21 but not p27. The mRNA stabilityof p53 was unaffected by PARN-depletion in both types of cells. A dramatic stabilizingeffect of PARN-depletion on p21 mRNA stability was observed in the AGS cells but notin the MKN28 cells. We further showed that the p21 3'-UTR triggered the action of *** difference observed in the MKN28 and AGS cells and various stress conditions suggested that the action of PARN strongly relied on the protein expression profiles, which led to heterogeneity in the stability of PARN-targeted mRNAs.

关键词： Poly(A)-specific ribonuclease cell cycle arrest p21 p53 mRNA stability tumorh eterogeneity

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The pathogenic role of Epithelial-mesenchymal transition(EMT) and related mechanism in diabetic retinopathy

The pathogenic role of Epithelial-mesenchymal transition(EMT...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者：周倜中山大学

Aims/hypothesis The fibrogenic process causes a traction force and the resultant detachmentof the retina makes Diabetic retinopathy a fibrotic disease as well. Epithelial-mesenchymal transition(EMT) played a role in the fibrosis in various organs. Therefore,the purpose of this study is to verify the occurrence of EMT and involved molecular mechanismin *** In vivo, EMT related marker expressions were evaluated by western blotting assayand immunohischemistry of retina of mice with streptozotocin-induced diabetes. In vitro,cultured retinal pigment epithelial cells and Müller cells were exposed to 30 mM L-glucose,D-glucose and D- glucose with different treatments. Western blotting assay, real-time PCRand immunochemistry were performed to determine β-catenin, N-cadherin, vimentin,snail1 and phos-ERK, phos-AKT expression. The cell migration, cell invision and cell viabilitywere evaluated using transwell assay and CCK8 *** The expression of E-cadherin was reduced and N-cadherin, Vimentin, β-cateninand alpha-SMA levels were significantly increased in the diabetic *** vitro, high glucose and advanced glycated end products elevated N-cadherin, Vimentin,β-catenin levels and decreased E-cadherin and zona occluding-1 levels in ARPE19 cells andMüller cells. The increased migration, invasion, cell viability and fibronectin promoted byhigh glucose were significantly reduced by N-cadherin-siRNA in ARPE19 cells. Mechanically,U0126 and AKT inhibitor significantly reduced the expression of N-cadherin and β-catenin as well as snail induced by high ***/interpretation Epithelial-mesenchymal transition was involved in the developmentof diabetic retinopathy and represents a new pathogenic mechanism of diabetic retinopathyand renders a new therapeutic target.

关键词： diabetic retinopathy hyperglycaemia Epithelial-mesenchymal transition(EMT)

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Overexpression of radish peroxidase results in enhance danthocyanin accumulation inducing by sugar in Arabidopsis thaliana

Overexpression of radish peroxidase results in enhance danth...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者： Linsong Wang Li Wang Xiao-lin Jia Xiang Wang Ying-ying Li Xi-ye Wang Jin-peng Su College of Life Sciences Henan Normal University

There has been increasing interest in anthocyanins due to anthocyanins potential nutritionalbenefits. Although the basic reactions of the anthocyanin biosynthetic pathways inplants have been analysed intensively, the regulation of their accumulation and fluxthrough the pathway has not been particularly well established. The aim of this study wasto use Arabidopsis thaliana overexpressing the radish peroxidase gene RsPRX1 to investigategene expression patterns associated with the accumulation of anthocyanins in Arabidopsisseedlings. Plants exposed to white light and a set of metabolic sugars(sucrose,glucose and fructose) showed an increase in anthocyanins content and number of compoundsin RsPRX1-overexpressing lines compared to the wild-type line when they weretreated with sucrose. There is superimposing effective in sucrose+glucose+fructose treatmentgroup compared with sucrose or glucose+fructose treatment groups. Peroxidaseactivity is ten times higher in transgenic Arabidopsis than in wild-type plants. Overexpressionof RsPRX1 strongly stimulates expression of anthocyanin regulatory genes(MYB75and bHLH(TT8)) and anthocyanin structural genes(CHS(chalcone synthase), LDOX(leucoanthocyanidin dioxygenase), DFR(dihydroflavonol 4-reductase)), and in the downregulatedexpression of endogenous FLS(flavonol synthase) and ANR(anthocyanidin reductase),but does not affect expression of the gene encoding sucrose transporter-1. Twobranches in the anthocyanin biosynthesis pathway have been proposed: FLS catalyses thereaction of dihydroquercetin to flavonols, and ANR catalyses the reaction of cyanidin toprocyanidin oligomers. It was concluded that a specific member of the peroxidase familyhas a role in regulating anthocyanin biosynthesis in response to sugar.

关键词： sugar,anthocyanin,peroxidase,overexpression,Arabidopsis thaliana,Rhaphanus sativus

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HSCARG Negatively Regulates the Cellular Antiviral RLR Pathwayby regulating TRAF3 Ubiquitination

HSCARG Negatively Regulates the Cellular Antiviral RLR Pathw...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者：彭炎炎 Ruidan Xu Xiaofeng Zheng State Key Lab of Protein and Plant Gene Research School of Life Sciences Peking University Department of Biochemistry and Molecular Biology School of Life Sciences Peking University

Innate immunity is critical for the host to defeat pathogen invasion, and aberrant activityof the immune response leads to immune-deficiency or autoimmune disease, thus identificationof the regulators involved in immune balance is particularly important. RIG-I likereceptors(RLRs) recognize cytosolic viral RNA and initiate innate immunity;they increasethe production of type I interferon(IFN) and the transcription of a series of antiviral genesto protect the host organism. Accurate regulation of the RLR pathway is important foravoiding tissue injury induced by excessive immune response. HSCARG is a newly identifiednegative regulator of NF-κB,here, we demonstrated that it participates in the precisenegative regulation of the innate immunity. HSCARG inhibits the cellular antiviral responsein an NF-κB independent manner, whereas its depletion has an opposite effect. In responseto viral infection, HSCARG interacts with TRAF3 and inhibits its ubiquitination bypromoting the recruitment of deubiquitinase OTUB1 to TRAF3. Knockout of HSCARG reducesthe de-ubiquitination of TRAF3 by OTUB1, and knockdown of OTUB1 abolishes theeffect of HSCARG. HSCARG also interacts with IKKεafter viral infection and impairs the associationbetween TRAF3 and IKKε, which further decreases the phosphorylation of IKKεand IRF3, thus suppresses the dimerization and nuclear translocation of IRF3. Moreover,knockdown of TRAF3 attenuates the inhibitory effect of IFN-β transcription by HSCARG,suggesting that TRAF3 is necessary for HSCARG to down-regulate RLR pathway. This studydemonstrated that HSCARG is a negative regulator that enables balanced antiviral innateimmunity, suggested that it is a potential target for the treatment of inflammatory andautoimmune diseases.

关键词： HSCARG TRAF3 OTUB1 ubiquitination cellular antiviral response

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Structure of a VLR-like protein Bf66946 from Branchiostoma floridae provides insights into the evolution of adaptive immune system in jawless vertebrates

Structure of a VLR-like protein Bf66946 from Branchiostoma f...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者：曹冬冬成望江永亮汪文捷李琼周丛照 Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences University of Science and Technology of China

With the increase of population with auto-immunity diseases today,more and more researchesare focused on the origination of adaptive immunity in *** characterizationof the variable lymphocyte receptors(VLRs)consisting of leucine-rich repeats(LRRs)in agnathans(jawless fish)has brought the origin of adaptive immunity forward to500 Mya ago when the vertebrate starts to ***,amphioxus at the basal positionof the chordate phylum was reported to hold extraordinary innate complexity and diversity,which was therefore named as"the explosion of immunity".Moreover,some researchershave found some evidence of the existence of adaptive immunity related moleculesin *** this study,we screened out nine LRR-only proteins from Branchiostomafloridae on the basis of sequence *** these proteins,the threedimensionalstructure of Bf66946 was determined at 1.60 ? resolution by X-ray *** and structural analysis reveals that Bf66946 is a VLR-like protein andshows homologous to VLRC rather than either VLRA or *** to the structure-known VLRs,Bf66946 also forms a horseshoe-shaped right-handed solenoidal ***,the CP in Bf66946 has an extra of 8 amino-acid residues and folds into aα-*** electrostatic potentials analysis displays an electron-negative region within theconcave surface of the LRR solenoid structure which is suggested as the ligand-bindingsite,implying its recognized ligand might be ***,the bacterialbinding assay showed that Bf66946 can attach to the surface of *** and ***(Gram-positive bacteria),but not to ***(Gram-negative bacteria).This observationsuggests that Bf66946 could recognize the ligands which are characteristically displayedon the surface of Gram-positive ***,the provided in our study gives insightsinto the existence of adaptive immunity in amphioxus,making a deep understandingto the evolution of adaptive immune system in j

关键词： Amphioxus leucine rich repeat(LRR)-containing proteins crystal structure evolution

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The effect of different iron on growth, protein nitration and metabolism in HepG2 cell:various reaction mechanism of iron and ROS/RNS

The effect of different iron on growth, protein nitration an...

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中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议

作者： Yan Xu Peng Xia Weike Ma Yuting Li Su Lv Ruijie Wang Hengyu Hu Basic Medical College of Zhengzhou University Zhengzhou University Nursing College of Zhengzhou University

In previous studies, iron has been shown to play a significant role in the formation of free radicals which contributed to oxidative stress, resulting in cell damage. Damage to cultured hepatocytes was prevented when the cells were preincubated with desferrioxamine,suggesting iron-dependent generation of ROS. Since there are several kinds of iron existing in human body system, it is very important to delineate the effect and various reaction mechanisms of different iron with RNS/ROS. Here, we present evidence that there are agreat diversity of mechanisms in iron reaction with RNS/ROS:(a) The MTT assay results showed that hemin could effectively induce HepG2 cell injury and the decrease of cell viability,while all the iron used would increase cell viability in relative low concentration. Ferritin,hemoglobin,ferric citrate and EDTA-Fe could not induce HepG2 cell injury even in relative high concentration.(b)With the same concentration of iron, NaNO2 and glucose oxidase(which could produce H2O2), there is difference in protein expression and protein modification,which suggested that there are vaious mechanism of different forms of iron.(c) In vitro methylene blue assay, it showed that hemin and hemoglobin were more power fulagents than the other three forms of iron in chemical oxidation of methylene blue,which means they has stronger capability in catalysing Fenton-like reaction to produce hydroxyradical. These result strongly suggest that there are various mechanisms of iron reaction with RNS/ROS, which is very useful for the research in I/R liver injury.

关键词： protein nitration HepG2 iron

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