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Signal transduction mediated by bid, a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways

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Cell Research 2000年第3期10卷 161-167页

作者： YIN XIAO-MING (Department of Pathology, University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15261, USA) Department of Pathology University of Pittsburgh School of Medicine Pittsburgh USA

Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.

关键词： Apoptosis Bcl-2 family proteins bid Fas TNF.

Expression of Bcl-2 inhibited Fas-mediated apoptosis in human hepatocellular carcinoma BEL-7404 cells

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Cell Research 2000年第3期10卷 233-242页

作者： CHANG YUN CHAO, YONG HUA XU (Shanghai institute of Cell Biology, Chinese Academy of Sciences, 320 Yue-yang Road, Shanghai 200031, China) Shanghai Institute of Cell Biology Chinese Academy of Sciences Shanghai China

Apoptosis plays an important role in embryonic development, tissue remodeling, immune regulation and tumor regression. Two groups of molecules (Bcl-2 family and 'Death factor' family) are involved in regulating apoptosis. In order to know about the effect of Bcl-2 on apoptosis induced by Fas, a typical member of 'Death factor' family, the transfection experiments with expression vectors pcDNA3-fl and pcDNA3-bcl-2 were performed in BEL-7404 cells, a human hepatocellular carcinoma cell line which expresses endogenous Fas, but not FasL and Bcl-2. The data showed that the expression of FasL in pcDNA3-fl transfected hepatoma cells obviously induced the apoptosis of the cells. However, the overexpression of Bcl-2 in pcDNA3-bcl-2 transfected 7404/b-16 cells counteracted pcDNA3-fl transient transfection mediated apoptosis. Further study by cotransfection experiments indicated that bid but not Bax (both were pro-apoptotic proteins of Bcl-2 family) blocked the inhibitory effect of Bcl-2 on Fas-mediated apoptosis. These results suggested that Fas-mediated apoptosis in human hepatoma cells is possibly regulated by Bcl-2 family proteins via mitochondria pathway.

关键词： Apoptosis FasL Bcl-2 bid Bax human hepa- tocellular carcinoma cells.

Fucoidan Induces G_1 Phase Arrest and Apoptosis through Caspases-dependent Pathway and ROS Induction in Human Breast Cancer MCF-7 Cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2013年第5期33卷 717-724页

作者： Amal M. Banafa Sadia Roshan 柳昀熠陈慧洁陈明洁杨广笑何光源 The Genetic Engineering International Cooperation Base of Ministry of Science and Technology Key Laboratory of Molecular Biophysics of Ministry of Education College of Life Science and Technology Huazhong University of Science and Technology

Fucoidan is an active component of seaweed, which inhibits proliferation and induces apoptosis of several tumor cells while the detailed mechanisms underlying this process are still not clear. In this study, the effect of Fucoidan on the proliferation and apoptosis of human breast cancer MCF-7 cells and the molecular mechanism of Fucoidan action were investigated. Viable cell number of MCF-7 cells was decreased by Fucoidan treatment in a dose-dependent manner as measured by MTT assay. Fucoidan treatment resulted in G1 phase arrest of MCF-7 cells as revealed by flow cytometry, which was associated with the decrease in the gene expression of cyclin D 1 and CDK-4. Annexin V/PI staining results showed that the number of apoptotic cells was associated with regulation of cytochrome C, cas- pase-8, Bax and Bcl-2 at transcriptional and translational levels. Both morphologic observation and Hoechst 33258 assay results confirmed the pro-apoptotic effect of Fucoidan. Meanwhile, the ROS pro- duction was also increased by Fucoidan treatment, which suggested that Fucoidan induced oxidative damage in MCF-7 cells. The results of present study demonstrated that Fucoidan could induce GI phase arrest and apoptosis in MCF-7 cells through regulating the cell cycle and apoptosis-related genes or proteins expression, and ROS generation is also involved in these processes.

关键词： Fucoidan MCF-7 cells apoptosis reactive oxygen species caspase-8 cytochrome C Bcl2 Bax bid

bid BH3 peptide,but not its mutant form G^(94)E, induces permeability transition pore opening and cytochrome c release in vitro

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Chinese Science Bulletin 2002年第7期47卷 553-557页

作者： XIATian, JIANG Chunsun, LI Linjiang, ZHANG Yong, JIN Haijing, LIU Shusen, WU Caihong & CHEN QuanThe National Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China The National Ke The National Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences Beijing China The National Key Laboratory of Biomembrane and Membrane Biotechnology Beijing University Beijing China Tianjin Institute of Sport Medicine Tianjin China

It has been shown that bid and its truncated form tbid could induce cytochrome c (cyt c) release without impacting on PTP. We first show that bid BH3 peptide, but not its mutant form of bid BH3 peptide G94E, which is unable to bind to Bcl-xL, induces permeability transition pore (PTP) opening in a dose dependent manner. bid BH3 peptide also induces the reduction of mitochondria membrane potential (Ψm) and cyt c release from mitochondrial in vitro. PTP opening and the loss of Ψm, were inhibited by Bcl-xL, cyclosporin A and ruthenium red, and the latter was an inhibitor of Ca2+ uniporter in the mitochondrial membrane. These results indicate that bid BH3 peptide could antagonize Bcl-xL to induced PTP opening and mitochondrial dysfunction.

关键词： apoplosis bid BH3 Bcl-xL mitochondria permeability transition pore.

bid在肾透明细胞癌中表达的预后价值及肿瘤微环境特征

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BID在肾透明细胞癌中表达的预后价值及肿瘤微环境特征

作者：曾加义南方医科大学

学位级别：硕士

目的目前的研究发现,BH3相互作用结构域死亡激动剂(BH3 interacting domain deathagonist,bid)与多种肿瘤的发生发展密切相关。然而,bid与肾透明细胞癌(clear cell renal cell carcinoma,ccRCC)相互作用的研究至今尚无明确报道,其在ccRC... 详细信息

目的目前的研究发现,BH3相互作用结构域死亡激动剂(BH3 interacting domain deathagonist,bid)与多种肿瘤的发生发展密切相关。然而,bid与肾透明细胞癌(clear cell renal cell carcinoma,ccRCC)相互作用的研究至今尚无明确报道,其在ccRCC中发挥的作用仍不清楚。本研究旨在探究bid在ccRCC中的表达情况,分析其表达对ccRCC的预后价值,为患者的风险评估和生存预测提供帮助;并探究其对肿瘤微环境(tumor microenvironment,TME)的影响,为开发新的免疫治疗靶点提供理论依据。方法从癌症基因组图谱(TCGA)数据库、国际肿瘤基因组协作组(ICGC)数据库以及基因表达综合数据库(GEO)获取了 ccRCC和正常肾组织的转录组信息和临床信息,并通过R语言软件对数据进行整理。首先,我们通过R包在ccRCC和正常肾组织中对bid的表达水平进行差异分析。随后,根据bid表达的中位数,将ccRCC患者分为高表达组和低表达组,并通过生存分析比较高表达组和低表达组之间总体生存期和无进展生存期的差异。然后,我们通过相关性分析评估了 bid的表达量与患者临床特征的关系。接下来,我们进行了单因素Cox回归分析和多因素Cox回归分析,以评估bid是否可以作为预测ccRCC患者预后的独立预后因素。之后,我们在训练队列中建立Cox风险预后模型,并在内部测试队列、GEO队列和ICGC队列中进一步验证模型的有效性和稳定性。我们还基于bid和临床信息构建了列线图,以进一步提高模型在临床中的实用性。此外,我们通过临床标本的转录组测序和免疫组化验证了生物信息学的结果。最后,我们通过GSEA富集分析、ssGSEA富集分析、ESTIMATE算法、CIBERSORT算法、TIDE评分等多种方法分析了 bid对TME的影响,以探究bid可能在ccRCC发生进展中的潜在机制。结果与正常肾组织相比,bid在ccRCC组织中高表达,临床标本的转录组测序数据和免疫组化染色验证了这一结果。与bid低表达的患者相比,bid高表达的患者总体生存期和无进展生存期更差。临床相关性分析表明,bid在男性病人中表达更高,bid的高表达预示更差的组织学分级和病理分期,且导致远处转移。单因素和多因素Cox回归分析表明bid是ccRCC的独立预后因素。基于bid的预后模型可以在不同队列中准确预测患者的预后。此外,bid的表达水平与PD-1、LAG3等多个免疫检查点分子密切相关。富集分析表明bid在免疫相关反应和代谢相关通路中显著富集。相关性分析结果显示,bid的表达与多种免疫细胞密切相关。bid高表达组具有高水平的免疫细胞浸润和免疫活性,并介导了不同的TME免疫浸润特征。结论bid在ccRCC中呈现高表达,是一种可靠的预测ccRCC预后的生物标志物,并与TME密切相关,可能是ccRCC患者免疫治疗的潜在靶点。

关键词： bid 肾透明细胞癌预后模型肿瘤微环境

Cyclopamine联合喜树碱诱导口腔鳞癌凋亡的机制

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南方医科大学学报 2010年第5期30卷 1034-1036页

作者：江穗陈锡林丁咏陈仲伟朱李军冯航王启朋甄茂川汪谦广东省人民医院广东省医学科学院口腔科广东广州510080 中山大学附属第一医院普通外科广东广州510080

目的研究Hedgehog通路特异性抑制剂cyclopamine联合喜树碱对口腔肿瘤细胞增殖、凋亡的影响。方法 CCK8法检测cyclopamine联合喜树碱对HSQ-89细胞增殖的影响;流式细胞仪检测cyclopamine联合喜树碱对HSQ-89细胞凋亡的影响;RT-PCR检测cyclo... 详细信息

目的研究Hedgehog通路特异性抑制剂cyclopamine联合喜树碱对口腔肿瘤细胞增殖、凋亡的影响。方法 CCK8法检测cyclopamine联合喜树碱对HSQ-89细胞增殖的影响;流式细胞仪检测cyclopamine联合喜树碱对HSQ-89细胞凋亡的影响;RT-PCR检测cyclopamine及喜树碱处理后HSQ-89细胞凋亡相关分子表达变化情况。结果 Cyclopamine联合喜树碱较单用喜树碱能更加明显抑制HSQ-89细胞活性。Cyclopamine处理后HSQ-89细胞中Bcl-2表达下降,而Bcl-xl、bid等表达不变,联合喜树碱后Bcl-2表达进一步减少。结论 Cyclopamine联合喜树碱能有效抑制Bcl-2表达而发挥抑制癌细胞增殖,并诱导凋亡效应。

关键词：口腔鳞癌信号转导凋亡 cyclopamine 喜树碱 Bcl-2 Bcl-xl bid

p-Akt、bid与小鼠局灶性脑缺血后处理保护作用的关系

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解剖学报 2011年第2期42卷 164-169页

作者：刘媛媛崔颖高俊玲田艳霞冉芳李冉崔建忠华北煤炭医学院基础医学部河北唐山063000 河北医科大学临床医学系石家庄050017 唐山市工人医院神经外科河北唐山063000

目的探讨p-Akt、bid在小鼠局灶性脑缺血再灌注(I/R)及缺血后处理(IP)后的启动规律,探讨p-Akt、bid与IP保护作用的关系。方法将315只雄性昆明小鼠采用线栓法建立大脑中动脉栓塞模型后,随机分成假手术组(Sham组)、缺血再灌注组(I/R组)、... 详细信息

目的探讨p-Akt、bid在小鼠局灶性脑缺血再灌注(I/R)及缺血后处理(IP)后的启动规律,探讨p-Akt、bid与IP保护作用的关系。方法将315只雄性昆明小鼠采用线栓法建立大脑中动脉栓塞模型后,随机分成假手术组(Sham组)、缺血再灌注组(I/R组)、缺血后处理组(IP组)、缺血后处理+PI-3K抑制剂LY294002组(IP+LY组)4组,于再灌注相应时间点取材,免疫组织化学方法检测p-Akt、bid的表达及分布情况;免疫印迹法检测皮质p-Akt、bid蛋白表达情况。氯化三苯基四氮唑(TTC)染色测定脑梗死体积。结果与Sham组比较,I/R组神经元胞质中可见p-Akt及bid的表达明显上调,p-Akt表达于30min增加,1 h达高峰(Pbid表达于6 h增加,24 h达高峰(Pbid表达明显降低(Pbid免疫反应性呈负相关(r=-0.8265,Pbid参与缺血后处理过程;缺血后处理可能通过PI-3K/Akt通路发挥脑保护作用;Akt可能通过死亡受体通路调控bid的表达。

关键词：缺血再灌注损伤缺血后处理 p-Akt bid 免疫组织化学免疫印迹法氯化三苯基四氮唑染色小鼠

表达促凋亡蛋白bid的重组耻垢分枝杆菌的构建及其对巨噬细胞凋亡的影响

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医学信息 2022年第23期35卷 41-49页

作者：逄亚宁杨国平孟余吴利先李光华大理大学基础医学院医学微生物与免疫学教研室

目的构建表达并分泌外源性促凋亡蛋白bid的重组耻垢分枝杆菌，并研究其对小鼠巨噬细胞RAW264.7凋亡的影响。方法运用生物信息技术对小鼠bid蛋白质的理化性质、分泌属性、保守结构域及蛋白相互作用网络等进行分析，应用无缝克隆技术及... 详细信息

目的构建表达并分泌外源性促凋亡蛋白bid的重组耻垢分枝杆菌，并研究其对小鼠巨噬细胞RAW264.7凋亡的影响。方法运用生物信息技术对小鼠bid蛋白质的理化性质、分泌属性、保守结构域及蛋白相互作用网络等进行分析，应用无缝克隆技术及传统酶切酶连方式构建pMV261-ASP(BamHI)-10His、pMV261-ASP(BamHI)-bid-10His、pMV261-ASP(EcoRI)-10His、pMV261-ASP(EcoRI)-bid-10His重组质粒，并电转化入耻垢分枝杆菌；通过BCA蛋白定量及免疫印迹技术分析蛋白表达情况，采用AnnexinV-FITC/PI双染法流式检测bid重组耻垢分枝杆菌对RAW264.7小鼠巨噬细胞凋亡的影响。结果小鼠bid蛋白是一种等电点为4.80的亲水性蛋白质，其中亮氨酸所占比例最高，为11.3%，色氨酸含量最低，为0.5%；二级结构中，α-螺旋（Hh）、无规则卷曲（Cc）、β-折叠（Ee）、β-转角（Tt）所占比例依次为65.13%、27.69%、4.10%、3.08%;bid蛋白不具有跨膜结构域及信号肽，属于非分泌性蛋白质，具有死亡保守结构域，可与Caspase8、Bcl-2、Granzyme B等凋亡相关蛋白发生相互作用；本次构建的ASP-bid重组耻垢分枝杆菌可以表达并分泌目标蛋白，且可增强RAW264.7小鼠巨噬细胞凋亡的比例。结论表达外源基因bid的重组耻垢分枝杆菌可以促进巨噬细胞凋亡发生，这可为新型结核病预防疫苗的研发提供新的思路与技术。

关键词：结核病耻垢分枝杆菌信号肽 bid 细胞凋亡

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微量酸类气体的分析

低温与特气 2022年第2期40卷 32-35页

作者：孙赟珑曲庆大连大特气体有限公司辽宁大连116021

酸类气体(例如乙酸)的极性很强,在分析定量的过程中面临诸多问题,采用岛津公司的bid检测器,利用不同浓度[(10~1000×10^(-6))(摩尔分数)]的乙酸标准气,对乙酸的吸附性、进样重复性、定量线性、检测限、分析条件等方面进行了深入探讨,为... 详细信息

酸类气体(例如乙酸)的极性很强,在分析定量的过程中面临诸多问题,采用岛津公司的bid检测器,利用不同浓度[(10~1000×10^(-6))(摩尔分数)]的乙酸标准气,对乙酸的吸附性、进样重复性、定量线性、检测限、分析条件等方面进行了深入探讨,为酸类气体的分析提供一定的指导方法。

关键词： bid 吸附性酸类气体标准气体乙酸