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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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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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Anticancer mechanism of DMAMCL, the dimethylamino Michaeladduct of micheliolide, on colorectal cancer cells in vitro and in vivo

Anticancer mechanism of DMAMCL, the dimethylamino Michaeladd...

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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：徐诚望袁守军军事医学科学院放射与辐射医学研究所

The incidence of colorectal cancer is the third cancer threatening human health. It hasbeen reported that micheliolide(MCL) could reduce the proportion of AML stem cells(CD34+CD38-) in primary AML cells. DMAMCL, the dimethylamino Michael adduct ofmicheliolide, slowly releases MCL in plasma and demonstrates remarkable therapeutic efficacyin the nonobese diabetic/severe combined immunodeficiency AML models. By CCK-8 and flow cytometry assays, we found that DMAMCL could dramatically inhibit the proliferationof several colorectal cancer cell lines including HCT116, HT29, and CLY. In addition,DMAMCL could induce apoptosis and G2/M phase arrest in these cell lines through enhancingthe expressions of activated caspase-3 and p21 respectively. When colorectal cancercells were treated with DMAMCL, we found that the sphere formation ability declined significantlyand the percentage of CD133 and CD44-positive cells decreased in serum-freemedia. In vivo studies revealed that DMAMCL inhibited tumors growth by reducing proportionof cancer stem cells in nude mouse models with HCT116 xenografts. Taken together,DMAMCL is a potential lead compound for development of antitumor drugs targetingcolorectal cancers.

关键词： DMAMCL Colorectal cancer

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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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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-409-3p suppresses colorectal cancer invasion andmetastasis through inhibition of GAB1

MicroRNA-409-3p suppresses colorectal cancer invasion andmet...

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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： Rongpan Bai Chunhua Weng Haojie Dong Siqi Li Guangdi Chen Zhengping Xu Institute of environmental Health Zhejiang University School of Medicine

Increasing evidence has shown that microRNAs(miRNAs) are involved in regulating tumordevelopment and progression. In this study, miR-409-3p was identified as a tumor suppressorin human colorectal cancer metastasis. MiR-409-3p expression was significantlydecreased in primary colorectal cancer tissues than in the paired normal tissues and it wasfound to be associated with tumor lymph node metastasis. Overexpression of miR-409-3pin CRC cells dramatically suppressed their migration and invasion in vitro and distal pulmonarymetastases in vivo. Further studies revealed that miR-409-3p suppressed the expressionof Grb2-associated binding protein(GAB1) by directly binding to its 3'-untranslated region. Silence of GAB1 could recapitulate the effects of miR-409-3p overexpression,while restoration of GAB1 in miR-409-3p overexpression CRC cells partially reversedthe miR-409-3p-mediated suppressive effects. Taken together, these results demonstrated that miR-409-3p suppressed CRC cells migration and invasion though directly targeting the GAB1 and provided a promising insight in developing novel diagnostic and therapeutic strategy for colorectal cancer treatment.

关键词： colorectal cancer microRNA-409-3p tumor metastasis GAB1

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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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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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Hsp90 inhibitor 17-AAG sensitizes Bcl-2 inhibitor (-)-gossypol by suppressing ERK-mediated protective autophagy and Mcl-1accumulation in hepatocellular carcinoma cells

Hsp90 inhibitor 17-AAG sensitizes Bcl-2 inhibitor (-)-gossyp...

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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： Bin Wang Zhenhong Ni Xinzhe Li Jiqin Lian Fengtian He Department of Biochemistry and Molecular Biology Third Military Medical University

Natural BH3-memitic(-)-gossypol((-)-Gos) shows promising antitumor efficacy in severalkinds of cancers, but it induces protective autophagy in hepatocellular carcinoma(HCC)cells, which leads to drug resistance. In the present study, we for the first time demonstratedthat Hsp90 inhibitor 17-AAG enhanced(-)-Gos-induced apoptosis via suppressing(-)-Gostriggered protective autophagy and Mcl-1 accumulation. The suppression effect of17-AAG on autophagy was mediated by ERK inactivation, which was not associated withthe instability of Beclin1 or LC3 protein. Morover, 17-AAG downregulated(-)-GostriggeredMcl-1 accumulation by inhibiting Mcl-1Thr163 phosphorylation and promotingprotein degradation. Collectively, Our study indicates that Hsp90 plays an important role intumor maintenance, and repression of Hsp90 may be a novel strategy for Bcl-2-targetedchemotherapies, especially for overcoming the drug resistance(This work was supportedby cstc2013jjB10015 and NSFC81273226).

关键词： (-)-Gossypol Bcl-2 Hsp90 Autophagy Apoptosis Mcl-1 ERK

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The UNC5D dependence receptor intracellular domain regulatespro-apoptotic transcription via nuclear translocation duringneuroblastoma regression

The UNC5D dependence receptor intracellular domain regulates...

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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： Yuyan Zhu Meng Yu Yixia Wang Yifu Chen Xiaojun Man Department of Urology First Hospital of China Medical University Department of Laboratory Animal China Medical University

Spontaneous regression of neuroblastoma(NB)resembles the developmentally regulatedprogrammed cell death(PCD)of sympathetic *** tumor cells express highlevels of the nerve growth factor(NGF)receptors TRKA and p75NTR and are dependent onNGF for survival;however,the underlying molecular mechanism remains ***,weshow that UNC5D,a dependence receptor that is directly targeted by p53 family members,is highly expressed in favorable *** withdrawal strongly upregulated UNC5D,E2F1,and p53 in human primary favorable *** induced UNC5D was cleaved by caspases2/3,and the released intracellular fragment translocated into the nucleus and interactedwith E2F1 to selectively transactivate the proapoptotic target *** cleavage ofUNC5D and its induction of apoptosis were strongly inhibited by addition of ***5d(-/-)mice consistently exhibited a significant increase in dorsal root ganglia neuronsand resistance to NGF depletion-induced apoptosis in sympathetic neurons compared withwild-type *** data suggest that UNC5D forms a positive feedback loop with p53 andE2F1 to promote NGF dependence-mediated PCD during NB regression.

关键词： dependence receptor UNC5D apoptosis neuroblastoma

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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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