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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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HBx induced elevation of cytoplasmic alpha-fetoprotein mediates hepatocarcinogenesis by blocking RAR regulated transcription of GADD45γ

HBx induced elevation of cytoplasmic alpha-fetoprotein media...

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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： Chao Zhang Gang Li peking university

The aim of this study was to gain a better understanding of the molecular mechanism underlyingthe previously unrecognized role of cytoplasmic AFP in RAR mediated transcriptionof GADD45α and the resulting biological effects during HBV induced *** of specimens from HCC patients showed that up-regulation of cytoplasmic AFP isassociated with down-regulation of GADD45α in neoplastic tissue. Assays based on hepatocytecell lines of differing AFP expression showed transfected HBx is able to promotethe transcription of AFP by acting on the promoter and enhancer in the AFP regulatory *** itself did not directly impact transcription of GADD45α. However, the obstructionof RAR signaling by HBx induced elevation of AFP led to down-regulation ofGADD45α. Cytoplasmic AFP was able to interact with RAR, disrupting its entrance into thenucleus and binding to the element in the regulatory region of the GADD45α gene. Knockdownof AFP in siRNA-transfected AFP positive cell lines was synchronously associatedwith an apparent incremental increase of RAR binding to DNA, as well as up-regulation ofGADD45α and vice versa in afp gene-transfected AFP negative cell lines. Conclusion: these findings provide a novel insight into the role of cytoplasmic AFP as a critical signal moleculein the RAR signal network during HBV induced hepatocarcinogenesis.

关键词： HBV hepatoma all trans retinoic acid nuclear receptor transcription regulation Abstract

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TMEM16A and myocardin form a positive feedback loop that isdisrupted by KLF5 during Ang Ⅱinduced vascular remodeling

TMEM16A and myocardin form a positive feedback loop that isd...

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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： Xin-hua Zhang Key Laboratory of Neural and Vascular Biology Department of Biochemistry and Molecular BiologyMinistry of Education Hebei Medical University

TMEM16A protein is recently identified as an important component of Ca+- dependentCl– channels(CaCCs) in vascular smooth muscle cells(VSMCs). However, the functions ofTMEM16 A protein and the mechanisms responsible for regulating TMEM16 A gene expressionin the vessels remain largely unclear. Here we showed that myocardin activatedTMEM16 A expression by forming a complex with SRF bound to the CArG of the TMEM16 Apromoter in VSMCs. Expression of myocardin and VSMC differentiation marker genes inturn was upregulated by TMEM16 A, forming a positive feedback loop to induce cell *** Ang Ⅱsignaling activation, KLF5 formed a complex with myocardin and inhibitedthe formation of myocardin-SRF complex on the CArG element of the TMEM16 Apromoter, subsequently leading to inhibition of TMEM16 A transcription and disruption ofthis feedback loop. These results indicate that KLF5 induced by Ang Ⅱ disrupts the positive feedback loop between myocardin and TMEM16 A, reverting VSMCs from differentiated tode differentiated phenotype, leading to vascular remodeling.

关键词： TMEM16A myocardin feedback loop Kruppel-like factor 5 vascular smoothm uscle cell

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Tumorigenic activity of human ribnuclease-4 in gliomas

Tumorigenic activity of human ribnuclease-4 in gliomas

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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： Jinghao Sheng Guangdi Chen Chi Luo Guo-fu Hu Zhengping Xu Research Center for Molecular Medicine Zhejiang University School of Medicine

Malignant gliomas are the most common and aggressive primary brain tumors with an extremelypoor prognosis and limited treatment options. Although substantial efforts havebeen devoted into glioma management, effective treatment is still lacking. Therefore, it isurgent to investigate the pathogenesis of malignant gliomas and seek for novel therapeutictargets. Through analysis of 430 cases of human gliomas with different disease stages,we found that the expression of human ribonuclease-4(RNASE4) was positively correlatedwith disease progression, with higher level of RNASE4 in higher degree of gliomas andpoorer survival rates. RNASE4 is the fourth member of the secreted and vertebrate-specificribonuclease superfamily. It has been revealed that RNASE4 played a role in neuroprotectiveactivity through promoting angiogenesis, neurogenesis, and neuronal survival understress. However, the molecular mechanism of RNASE4 in glioma progress remains to beelucidated. Here we have identified that RNASE4 was necessary for the proliferation ofglioma cells in vitro and xenograft tumor growth, angiogenesis and metastasis in nudemice. We also found that the tumor-promoting effect of RNASE4 depended on its ribonuclease activity, suggesting the importance of the ribonucleolytic activity in the progression of gliomas. Since RNASE4 is a secreted protein and can be easily targeted, our finding would shed light on the development of novel the rapeutic strategy of malignant gliomas.

关键词： Ribonuclease-4 Gliomas Ribonucleolytic activity RNA metabolism

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Suppression of Akt/mTOR pathway Enhances (-)-Gossypol-Induced Cytotoxicity in Androgen Independent Prostate Cancer Cells

Suppression of Akt/mTOR pathway Enhances (-)-Gossypol-Induce...

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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： Jiqin lian Zhenhong Ni Bin Wang Fengtian He Third Military Medical University

The natural BH3-mimetic(-)-gossypol is currently undergoing Phase II-III clinical trials forhuman prostate cancer and showing promising efficacy. Here we show that suppression ofAkt/mTOR pathway by NVP-BEZ235 significantly enhanced(-)-gossypol-induced cytotoxicityin androgen-independent prostate cancer cells(AI-PC cells) in vitro and in vivo. Ourdata indicated that(-)-gossypol and NVP-BEZ235 induce cell death via two distinct pathwaysin two different AI-PC cells. Intrinsic apoptotic pathway was preferentially activated inDU145 cells characterized with high ratio of proapoptotic to anti-apoptotic proteins andlow level of critical autophagy-related proteins, whereas autophagic pathway was preferentiallystimulated in PC-3 cells characterized with low ratio of pro-apoptotic to antiapoptoticproteins and high level of critical autophagy-related proteins. Furthermore, NVPBEZ235attenuates(-)-gossypol-activated Akt/mTOR pathway, thus it serves as a potentchemosensitizer to suppress cancer-initiating cell population in AI-PC cells. Taken together,our results expose a new action and the corresponding mechanism for NVP-BEZ235 asan enhancer of(-)-gossypols-induced cytotoxicity in both tumor-initiating and differentiatedcell populations.

关键词： (-)-Gosssypol NVP-BEZ235

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The inhibitory kinetics of 4-hydroxy cinnamic acid on mushroom tyrosinase from Agaricus bisporus

The inhibitory kinetics of 4-hydroxy cinnamic acid on mushro...

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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：胡泳华崔沂高焕娟许炼余新元王勤陈清西厦门大学生科院

Agaricus bisporus is one of the most important farm products in our country andone of the most vulnerable to browning vegetables after harvest due to their physiologicalactivities and organizational structure *** is the main reason ***,it is important to search an efficient and simple preservation method inorder to inhibit *** tyrosinase from Agaricus bisporus was purified by extraction with 0.1 mol/L PBS buffer(pH 6.8)and ammonium sulfate fractionation,then chromatography on Sephacryl S200followed by DEAE Sepharose *** purified enzyme determined to be homogeneousby polyacrylamide gel electrophoresis(PAGE).The specific activity of the purified enzymewas 5340 U/*** inhibition of 4-hydroxy cinnamic acid on the diphenolase activity of tyrosinase was *** IC50 of 4-hydroxy cinnamic acid was 1.10 mmol/*** it displayed a competitivemechanism,the inhibition constant was determined to be0.67 mmol/*** inhibitorykinetics of 4-hydroxy cinnamic acid on tyrosinase has been studied using the kineticmethod of substrate *** results showed that the inhibition of tyrosinase by 4-hydroxy cinnamic acid is a slow,reversible reaction with fractional remaining *** orderto understand the binding mode of 4-hydroxy cinnmic acid with PPO3(2Y9W),it wasdocked at the active site of PPO3 using *** result showed that Val283、His259、Phe264、Asn260and His85 residues were responsible for the interaction of the enzymewith 4-hydroxy cinnamic acid.

关键词： tyrosinase 4-hydroxy cinnamic acid inhibitory kinetics molecular dock

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Structural insights into SraP-mediated Staphylococcus aureus adhesion to host cells

Structural insights into SraP-mediated Staphylococcus aureus...

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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：江永亮杨益虎张娟王雷柏晓辉任艳敏李娜龚庆国梅一德张志勇薛挺张敬仁陈宇星周丛照 School of Life Sciences University of Science and Technology of China Shanghai Institute of Biochemistry and Cell Biology Center for Infectious Disease Research School of Medicine Tsinghua University

Staphylococcus aureus,a Gram-positive bacterium causes a number of devastating humandiseases,such as infective endocarditis,osteomyelitis,septic arthritis and ***,a surface-exposed serine-rich repeat glycoprotein(SRRP),is required for the pathogenesisof human infective endocarditis via its ligand-binding region(BR)adhering to *** remains unclear how SraP interacts with human *** we report the2.05crystal structure of the BR of SraP,revealing an extended rod-like architecture offour discrete *** N-terminal legume lectin-like module specifically binds to *** second module adopts aβ-grasp fold similar to Ig-binding proteins,whereas the last two tandem repetitive modules resemble eukaryotic cadherins butdiffer in calcium coordination *** the conditions tested,small-angle X-ray scatteringand molecular dynamic simulation indicated that the three C-terminal modulesfunction as a relatively rigid stem to extend the N-terminal lectin module ***-guided mutagenesis analyses,in addition to a recently identified trisaccharide ligandof SraP,enabled us to elucidate that SraP binding to sialylated receptors promotes *** to and invasion into host epithelial *** findings have thus provided novelstructural and functional insights into the SraP-mediated host-pathogen interaction of ***.

关键词： Staphylococcus aureus serine-rich repeat glycoprotein crystal structure hostpathogen interaction

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Silencing Gastrin Inhibits Cellular Proliferation, Migration andInvasion in Gastrin Cancer Cells

Silencing Gastrin Inhibits Cellular Proliferation, Migration...

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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： Jianjiang Zhou Yuan Xie Yan Zhao Yi Zeng Key Laboratory of Molecular Biology of Guiyang Medical College Key Laboratory of Molecular Biology of Guiyang Medical College

The gastrin secreted by gastric cancer cells was closely related to the development andprogression of gastric cancer. To study the effects of gastrin on cellular proliferation, migrationand invasion of gastric cancer cells, we constructed a eukaryotic expression vectorexpressing siRNA expression cassettes to gastrin and transfected it into gastric cancer cellsAGS. After successful establishment of the stable gastrin-silenced cell line AGS/Gas-siRNA,MMT assay, colony forming assay, cell wound healing assay and Transwell assay were usedto detect the proliferation, migration and invasion of the gastrinsilenced cells *** concentrations of matrix metalloproteinases-2(MMP-2) and vascular endothelialgrowth factor(VEGF) in culture medium of transfected cells were measured by ELISA. Theresults showed that, compared with the control cells with empty vector transfection, therelative proliferation rate and colony formation rate in soft agar were significantly decreasedin the gastrin-silenced cells. The cells migrated or invaded to the lower surface ofTranswell were reduced by 31.6 % and 34 % respectively. The concentrations of MMP-2and VEGF in medium of gastrin-silenced cells were lower than that in control cells. The resultssuggested that, after silenceing gastrin, the cellular proliferation, migration and invasionwere inhibited by reducing the secretion of MMP-2 and VEGF, which may be the molecular mechanism of promoting the invasion and metastasis of gastric cancer cells bygastrin.

关键词： gastrin gastric cancer migration invasion RNA interference

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Disruption of human vigilin impairs chromosome condensationand segregation

Disruption of human vigilin impairs chromosome condensationa...

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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： ling wei Xiaoyan Xie Junhong Li Shuwang Duan Yajun Ge Ran Li Wenyan Shen Wenli Yang Qiuying Liu Qiang Fu Yang Qin Department of Biochemistry and Molecular Biology West China School of Preclinical and Forensic Medicine Sichuan University Sichuan University“985 project-science and technology innovation platform for novel drug development”

Appropriate packaging and condensation are critical for eukaryotic chromatin’s accommodationand separation during cell *** vigilin,a multi-KH-domain nucleicacid binding protein,is associated with alpha satellites of ***1,a vigilin’shomolog,is implicated with chromatin condensation and *** expression ofvigilin was previously reported to elevate in highly proliferating tissues and increased in asubset of hepatocellular carcinoma *** studies showed that vigilin contributesto regulation of imprinted genes Igf2/H19 and colocalizes with HP1αon heterochromaticsatellite 2 andβ-satellite *** studies indicate that human vigilin might beinvolved in chromatin remodeling and regular cell *** investigate the potential roleof human vigilin in chromosomal condensation and segregation,the dynamic expressionof vigilin during cell cycle of HepG2 cells was *** endogenous vigilin highlyexpressed both in G1 and G2 phases,whereas low in S *** of human vigilinby RNA interference in HepG2 cells resulted in chromosome undercondensation and variouschromosome defects during mitotic phase,including chromosome misalignments,laggingchromosomes and chromosome *** polyploid nucleus in telophase wasalso *** the abnormal staining pattern of chromosomes,the shape of spindlewas ***,the chromatin showed a greater sensitivity to MNase ***,our findings show that human vigilin apparently participates in chromatincondensation and segregation.

关键词： Vigilin Chromosome Segregation Condensation

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Systematic Identification of Arsenic Binding Proteins Revealed that Warburg Effect is Disturbed by Arsenic

Systematic Identification of Arsenic Binding Proteins Reveal...

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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：张海南杨丽娜陶生策上海交通大学

Arsenic（ATO） is highly effective for treating acute promyelocytic leukemia（APL）,it may also be potentially effective for many other tumors. To explore this potential, it isnecessary to understand the MOA of arsenic's antitumor activity, and the first essentialstep is to identify the direct targeting proteins of arsenic. In this study, applying a humanproteome microarray carries 16, 368 human proteins, we developed a proteome microarraybased strategy for the identification of arsenic binding proteins on a systems level, andsuccessfully identified 360 arsenic binding proteins, which represent a wide range of biologicalfunctions. As a comparison, there are only 0 human proteins which are known arsenicbinders prior to this study. These proteins represent a wide range of biological *** the arsenic binding proteins, we identified a high confident arsenic binding motifwith vicinal thiol. Unexpectedly, proteins of glycolysis（Warburg effect） were highly enrichedof the newly identified arsenic binding proteins. We then focus on HK2. The bindingof arsenic to HK2 were confirmed, Cys256 and Cys 704 were identified as the binding *** studies showed that the activity of HK2 could be inhibited upon the addition ofarsenic both in vitro and in vivo. The strategy that we developed could be readily adoptedfor the study of other compound. The identified arsenic binding proteins could serve as avaluable resource for future MOA study, and the developing of novel synergistic therapeuticstrategies for treating solid tumors.

关键词： arsenic human protein microarray Warburg Effect

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Viral protein-repressed microRNA-148a controls tumor growthand metastasis through HPIPmediated mTOR signaling

Viral protein-repressed microRNA-148a controls tumor growtha...

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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： Xiaojie xu Zhongyi Fan Lei Kang Qinong Ye Beijing Institute of Biotechnology Peking University First Hospital

MicroRNAs(miRNAs) have been shown to be dysregulated in virus-related ***, cellular miRNA pathways regulating virus-related cancer development and progressionremain poorly understood. Here we report that the miR-148a/HPIP/mTOR pathwaycontrols virus-associated tumor growth and metastasis. By directly targeting hematopoieticpre-B cell leukemia transcription factor-interacting protein(HPIP), miR-148 a reducedHPIP expression, which led to repression of protein kinase B(AKT) and extracellularsignal-regulated kinase(ERK) and subsequent inhibition of the mammalian target of rapamycin(mTOR) signaling. The miR-148a/HPIP axis regulated mTOR expression through theAKT/ERK-FOXO4-ATF5 pathway. Hepatitis B virus(HBV) X protein(HBx) repressed cellularmiR-148 a and activated HPIP through interaction with the p53 tumor suppressor. MiR-148 a reduced the growth, epithelial-to-mesenchymal transition(EMT), invasion and metastasisof HBx-expressing hepatocarcinoma cells through inhibition of HPIP-mediated mTORsignaling. Moreover, expression of miR-148 a was down-regulated in HBV-related livercancer patients, and negatively correlated with HPIP, which was up-regulated in liver cancerpatients. Thus, miR-148 a activation or HPIP inhibition may be a useful strategy for cancer treatment.

关键词： MiR-148a HPIP mTOR signaling HBx

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