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Changes of lncRNAs and Related Genes in minor and major β-thalassemia

Changes of lncRNAs and Related Genes in minor and major β-t...

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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：马竞深圳宝安区妇幼保健院复旦大学

Most β-thalassemia are caused by β-globin gene mutations, while it comprehend clinicallyvery heterogeneous group of thalassemia-like disorders, ranging in severity from theasymptomatic state to the severe transfusion-dependent type. Recently, an increasingnumber of researches suggested that epigenetic changes anticipated the occurrence anddevelopment of β-thalassemia. In order to investigate if lncRNAs expressed differentially inβ-thalassemia, we collected 30 β-thalassemia major and 30 β-thalassemia carrier statesamples, matched with 30 normal controls. With abundant and varied probes accountingfor 33,045 lncRNAs in Arraystar Human lncRNA Microarray assay, 28,443 lncRNAs thatwere expressed at a specific level were detected. Compared with normal control, 1424 lncRNAs were identified up-regulated and 2045 downregulated in β-thalassemia major,623 lncRNAs were identified up-regulated and 349 down-regulated in β-thalassemia carrierstate. Compared with β-thalassemia carrier state, 1367 lncRNAs were identified upregulatedand 2356 lncRNAs downregulated in all β-thalassemia major samples. Rankingthe expression level of lncRNAs based on the microarray results, we selected 5 lncRNAs toanalyze the relationship between lncRNAs and β-thalassemia. DQ583499, Xist, LincRNA-TPM1,MRFS16P and LincRNA-RUNX2-2 were evaluated using qPCR in all samplesand the results were consistent with those of the microarray assay. This study implicatedthat the abnormal expression of lncRNAs in β-thalassemia may be correlated with variantclinical phenotypes.

关键词： lncRNAs β-thalassemia

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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： lie wang 浙江大学基础医学院免疫所

The interplay between the CD4-lineage transcription factor ThPok and the CD8-lineagetranscription factor, runt-related transcription factor 3(Runx3), in T-cell development hasbeen extensively documented. However, little is known about the roles of these transcriptionfactors in invariant natural killer T(iNKT) cell development. CD1d-restricted iNKT cellsare committed to the CD4(+)CD8(-) and CD4(-)CD8(-) sublineages, which respond to antigenstimulation with rapid and potent release of T helper(Th) 1 and Th2 ***, previous reports have demonstrated a new population of CD8(+) NKT cells inThPok-deficient mice. In the current study, we sought to determine whether Runx3 was involvedin the re-expression of CD8 and function of iNKT cells in the absence of ThPok. Weused mice lacking Runx3, ThPok or both and verified that Runx3 was partially responsiblefor the appearance of CD8(+) iNKT cells in ThPok knockout mice. Additionally, Runx3 participatedin the immune response mediated by iNKT cells in a model of α-galactosylceramide-induced acute hepatitis. These results indicate that Runx3 is crucial forthe phenotypic and functional changes observed in ThPok-deficient iNKT cells.

关键词： NKT cell development Transcription factor

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Research Progress in PEGylation of Drugs

Research Progress in PEGylation of Drugs

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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：宋新蕾山东大学药学院

Poly(ethylene glycol)(PEG)is a linear polyether diol with many useful properties such asnon-toxic,non-immunogenic,nonantigenic,highly soluble in water and FDA *** that was generally defined as the covalent attachment of activated PEG polymersto therapeutic agents is one of the most promising techniques to improve the pharmacokinetic,pharm acodynamic,and immunological profiles,and thus,enhance the therapeuticeffect of *** first-generation PEG chemistry was restricted to the use of low molecular weight linearPEGs,unstable linkages and lack of selectivity in *** the diol content ofcommercially available PEGs was high which leads to the inevitable presence of deactivatedPEG impurities and cross-linked protein *** second generation of PEG chemistry was designed to avoid the problems of first *** molecular weight of PEGs is higher,and in addition to the linearstructure,branched PEGs,forked PEGs and multi-armed PEGs are *** PEGs,which are PEGs bearing dissimilar terminal groups,are used in avariety of ways that includes linking macromolecules to surfaces for immunoassays,targetingof drugs,liposomes and viruses to specic tissues,liquid phase peptide synthesis andmany *** availability of PEGs with different molecular weights and activation formscan meet the various drug-modification *** PEGylation has become an established and highly rened technology by movingforward from initial simple random coupling approaches to site-selective PEGylation thatallow the obtainment of a single isomer,thus highly increasing the degree of homogeneityand the preservation of *** N-terminus and free cysteines were the rst sitesexploited for selective PEGylation but currently further positions can be addressed thanksto approaches like bridging PEGylation,enzymatic PEGylation,glycoPEGylation and PEGchemistry for oxidized carbohydrates or ***

关键词： PEGylation site-specific reversible

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Tanshinone suppresses AURKA through up-regulating theexpression of miR-32 in NSCLC

Tanshinone suppresses AURKA through up-regulating theexpress...

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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： zhongliang ma bingjie zhang detao wang xue li jiali wei botao zhao youxin jin School of life sciences Shanghai University School of Life Sciences Shanghai University State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Institutes for Biological SciencesChinese Academy of Sciences

Tanshinone, including tanshinone I(T1), tanshinone IIA(T2A), cryptotanshinone(CT), is theliposoluble constituent of Salia miltiorrhiza which has favourable medicinal value. Tanshinonemolecules can inhibit the growth of lung cancer cells in vitro, but its mechanism isstill unclear. AURKA, an oncogene, encodes a serine-threonine kinase which regulates mitoticprocesses in mammalian cells. Here, we report that tanshinone mediates AURKA suppressionpartly through up-regulating the expression of miR-32. We found that tanshinonecould inhibit cell proliferation, promote apoptosis and impede cell-cycle progression thusperforming an antineoplastic function in non-small cell lung cancer(NSCLC). As reported,tanshinone might attain these effects partly by down-regulating AURKA and such was thefact demonstrated by us. Results showed that AURKA gene knocked-down by siRNA couldmake similar effects in NSCLC. We also verified that AURKA was the target of miR-32. Inconclusion, our results demonstrated that tanshinone could inhibit NSCLC by upregulating the expressions of miR-32 and other related miRNAs to suppress AURKA.

关键词： Tanshinone AURKA miRNA NSCLC

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A primary study on mutation of HPRT exposure to γ ray andbenzo-pyrene

A primary study on mutation of HPRT exposure to γ ray andbe...

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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：刘建功 Hong-yan LIU Xu-hong DANG China Institute for Radiation Protection

Objective To investigate the changes of mutation of HPRT exposure to γ ray and benzopyrene,in order to try to find new differential diagnosis methods for cell injury induced byγ ray and benzo-pyrene. Methods Human peripheral blood samples from three personswere exposed to 60 Co γ-rays at 10 different doses(0-5Gy) and benzo-pyrene at 6 differentconcentrations(0-10μg/ml), its DNA was isolated from white cell. The changes of mutationof HPRT exposure to γ ray and benzo-pyrene were detected by real-time quantitative *** The relationship between mutation frequency of HPRT and irradiation dose represen tscertainline correlation from 0～5Gy, alinearregressionequa-tion(y=0.4298+0.0823 x,P<0.01,R2=0.93) has been obtained using statistics regressionanalysis software, while, the relationship between mutation frequency of HPRT and differentconcentrations(0-10μg/ml) represents no statistical significance,which was obtainedusing statistics software as(y=0.4200+0.0019 x, P>0.05, R2=0.450). There is an obvious influenceon mutation frequency of exon 5 of HPRT induced byγray,while there is no obvious influence on mutation frequency of exon 5 of HPRT induced by benzo-pyrene,which may be a new differential diagnosis index in the future.

关键词： γ ray benzo-pyrene mutation frequency HPRT

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The structural basis of RKIP binding with its substrate Raf-11-147

The structural basis of RKIP binding with its substrate Raf-...

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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： Chenyun Chenyun Guo Zhihua Wu Cuiping Fu Lu Ruan Lina Shi Donghai Lin Xiamen Univeristy

Raf1 kinase inhibitor protein(RKIP)directly interacts with Raf1 kinase,thereby regulatingthe Raf1/MEK/ERK pathway which is vital for cell growth and ***,little is known about the molecular mechanism of RKIP binding with *** N-terminaldomain of human Raf1(hRaf11-147aa)and human RKIP(hRKIP)were recombinant preparedhere and GST pull down experiment suggests an interplay involving hRaf11-147aaand hRKIP.15N-1H HSQC NMR experiments show hRaf11-147aa binds with hRKIP at itsconserved ligand-binding pocket,loop"127-149",and the C-terminal *** dissociationconstant is 6.49±0.39μM determined by exogenous fluorescent experiments.D70,D72,E83,Y120,and Y181 were further verified as key residues for hRKIP binding withhRaf11-147aa by site-directed *** G143-R146 was critical for the interactionof RKIP and Raf1,whose deletion causes binding affinity decreasing around *** results can provide important structural clue for designing lead compound by disruptingthe RKIP-Raf1 interaction.

关键词： RKIP Raf1147aa Binding sites

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MicroRNA-346 Mediates Tumor Necrosis Factor-■-induced Down-Regulation of Vitamin D Receptor in Gut Epithelial Cells

MicroRNA-346 Mediates Tumor Necrosis Factor-■-induced Down-...

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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： yunzi chen 南京医科大学

We recently reported that the gut epithelial vitamin D receptor(VDR) signaling inhibitscolitis through inhibition of intestinal epithelial cell apoptosis, and the level of colonic epithelialVDR is markedly down-regulated in patients with inflammatory bowel diseases(IBD), butthemechanism underlying VDR down-regulation in IBD is unknown. Here we showed thatTNF-αsuppresses VDR expression while simultaneously up-regulating miR-346 in human coloncancercells. Further studies demonstrated that miR-346 inhibits VDR by a specific target sequenceinthe 3' untranslated region of the human VDR transcript, and blockade of miR-346 with ahairpininhibitor abrogates the ability of TNF-α to inhibit VDR. These results indicate that TNF-αdownregulates VDR by inducing miR-346. Consistently, in human IBD biopsies the reductionofepithelial VDR is associated with increased immune cell infiltration and elevation of TNF-αandmiR-346. In an experimental model of colitis mucosal VDR expression is reduced over timewiththe progression of colitis, inversely correlated with the induction of TNF-α and miR-346 inthemucosa. Together these data suggest that during mucosal inflammation TNF-α inducesmiR-346, which down-regulates epithelial VDR. Mucosal VDR reduction in turn compromisestheintegrity of the mucosal epithelial barrier, further driving mucosal inflammation and colitisdevelopment.

关键词： microRNA-346 vitamin Dreceptor

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Study on the Importance of the Interaction of AZI-1 and AZ-1 in the Polyamine Pathway

Study on the Importance of the Interaction of AZI-1 and AZ-1...

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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： Bo Li Sen Liu Institute of Molecular Biology China Three Gorges University

The polyamines are small basic molecules essential for cellular proliferation and *** levels of polyamines are associated with several human diseases and diverse cancers,and the enzyme activity is related to the beginning and successive development of neoplasticdiseases. An autoregulatory circuit that responds to the intracellular level ofpolyamines regulates their production. In the center of this circuit is a family of small proteinstermed antizymes. Antizymes themselves are regulated at the translational level bythe level of polyamines. Antizymes bind ornithine decarboxylase(ODC) subunits and targetthem to ubiquitin-independent degradation by the 26 S proteasome. In addition, antizymesinhibit polyamine transport across the plasma membrane via an as yet unresolved *** may also interact with and target degradation of other growthregulatingproteins. An inactive ODC-homologous protein termed antizyme inhibitor regulatespolyamine metabolism by inhibiting antizymes' function. The ability of antizymes todegrade ODC, inhibit polyamine uptake and consequently suppress cellular proliferationsuggests that they act as tumor suppressors, while the ability of antizyme inhibitors tocounteract antizyme function indicates their growth-promoting and oncogenic *** this study, we designed a series of antizyme inhibitor-1(AZI-1) mutants that can not inhibitAZ-1, but do not affect the other functions of AZI-1. To observe the effects of AZI-1mutants' over-expression on cellular proliferation without acting on AZ-1, we hope tofind out a new role of AZI-1 in regulating cancer proliferation found in our previous study.

关键词： Polyamine Ornithine decarboxylase Antizyme Antizyme inhibitor

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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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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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