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| 1 | Wnt/Ca^2+ signaling pathway: a brief overview显示文摘表明串联的不在经典中的 Wnt/Ca2+ 少些比他们的正规对应物被描绘, Wnt/-catenin 小径。表明小径的不在经典中的 Wnt 是多样的,定义为发信号的 planer 房间极性小径, Wnt-RAP1 发信号小径, Wnt-Ror2 发信号小径, Wnt-PKA 小径, Wnt-GSK3MT 小径, Wnt-aPKC 小径, Wnt-RYK 小径, Wnt-mTOR 小径,和 Wnt/calcium 小径。所有这些小径展出在他们之间的重叠的可观的度。表明小径的 Wnt/Ca2+ 在开发作为一个关键调停人被译解。然而,在那里的现在是发信号的串联涉及许多另外的分子的现象的实质的证据。Wnt/Ca2+ 小径的许多方面是还神秘的。这评论将给表明小径的 Wnt/Ca2+ 的基本、演变的概念的简短概述。 | Antara De | 2011 | Acta Biochimica et Biophysica Sinica2011，43，10： | 66 |
| 2 | Wnt/b-catenin signaling plays an ever-expanding role in stem cell self-renewal,tumorigenesis and cancer chemoresistance显示文摘Wnt signaling transduces evolutionarily conserved pathways which play important roles in initiating and regulating a diverse range of cellular activities,including cell proliferation,calcium homeostasis,and cell polarity.The role of Wnt signaling in controlling cell proliferation and stem cell self-renewal is primarily carried out through the canonical pathway,which is the best-characterized the multiple Wnt signaling branches.The past 10 years has seen a rapid expansion in our understanding of the complexity of this pathway,as many new components of Wnt signaling have been identified and linked to signaling regulation,stem cell functions,and adult tissue homeostasis.Additionally,a substantial body of evidence links Wnt signaling to tumorigenesis of cancer types and implicates it in the development of cancer drug resistance.Thus,a better understanding of the mechanisms by which dysregulation of Wnt signaling precedes the development and progression of human cancer may hasten the development of pathway inhibitors to augment current therapy.This review summarizes and synthesizes our current knowledge of the canonical Wnt pathway in development and disease.We begin with an overview of the components of the canonical Wnt signaling pathway and delve into the role this pathway has been shown to play in stemness,tumorigenesis,and cancer drug resistance.Ultimately,we hope to present an organized collection of evidence implicating Wnt signaling in tumorigenesis and chemoresistance to facilitate the pursuit of Wnt pathway modulators that may improve outcomes of cancers in which Wnt signaling contributes to aggressive disease and/or treatment resistance. | Maryam K.Mohammed Connie Shao Jing Wang Qiang Wei Xin Wang Zachary Collier Shengli Tang Hao Liu Fugui Zhang Jiayi Huang Dan Guo Minpeng Lu Feng Liu Jianxiang Liu Chao Ma Lewis L.Shi Aravind Athiviraham Tong-Chuan He Michael J.Lee | 2016 | Genes & Diseases2016，3，1： | 70 |
| 3 | Wnt信号通路:调控机理和生物学意义显示文摘Wnt信号通路作为一种在进化中高度保守的信号通路,在生长、发育、代谢和干细胞维持等多种生物学过程中发挥重要作用。而Wnt通路的失控与癌症、肥胖和糖尿病等疾病的发生有密切联系。经典Wnt通路的调控过程,主要围绕beta-Catenin和TCF这两个关键调节因子进行,从而在转录水平上影响着大量与生长和代谢相关的靶基因的表达。本文将综合介绍近年来针对经典Wnt通路调控机理的研究进展,以及Wnt通路与疾病发生的关系。 | 尹定子 宋海云 | 2011 | 中国细胞生物学学报2011，33，2： | 60 |
| 4 | Role of the Wnt/β-catenin pathway in gastric cancer: An indepth literature review显示文摘Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas.The aberrant activation of the Wnt/β-catenin signaling pathway is involved in the development and progression of a significant proportion of gastric cancer cases. This review focuses on the participation of the Wnt/b-catenin pathway in gastric cancer by offering an analysis of the relevant literature published in this field. Indeed, it is discussed the role of key factors in Wnt/β-catenin signaling and their downstream effectors regulating processes involved in tumor initiation, tumor growth, metastasis and resistance to therapy. Available data indicate that constitutive Wnt signalling resulting from Helicobacter pylori infection and inactivation of Wnt inhibitors(mainly by inactivating mutations and promoter hypermethylation) play an important role in gastric cancer. Moreover, a number of recent studies confirmed CTNNB1 and APC as driver genes in gastric cancer. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput 'omics' approaches will help in the search for Wnt pathway antagonist in the near future. | Miguel Angel Chiurillo | 2015 | World Journal of Experimental Medicine2015，5，2： | 58 |
| 5 | 丹参酮ⅡA对COX-2激活Wnt/β-catenin信号通路介导的人肠癌细胞VEGF表达的调控作用显示文摘目的:探讨丹参酮ⅡA通过环氧化酶-2(COX-2)-Wnt/β-catenin信号通路调控人肠癌细胞血管内皮生长因子(VEGF)表达的作用机制。方法:分别采用PGE2和COX-2选择性抑制剂NS-398上调及抑制LoVo细胞COX-2表达,Western Blot检测COX-2对β-catenin蛋白表达的影响;分别采用丹参酮ⅡA、PGE2和/或GSK-3β选择性抑制剂SB-216763作用人肠癌HCT-116细胞24h,Western Blot法检测丹参酮ⅡA对COX-2和β-catenin蛋白表达的影响;ELISA法检测丹参酮ⅡA对VEGF表达的影响。结果:与对照组比较,PGE2能够显著上调LoVo细胞中COX-2蛋白表达,同时显著上调β-catenin在细胞总蛋白、浆蛋白和核蛋白中的表达水平;反之,COX-2抑制剂NS-398能够显著下调COX-2和β-catenin蛋白表达水平。丹参酮ⅡA能够显著下调COX-2和β-catenin蛋白在人肠癌LoVo细胞中表达水平,并且能够显著下调PGE2诱导的COX-2和β-catenin蛋白的高表达;同时,丹参酮ⅡA能够显著下调人肠癌LoVo细胞VEGF表达水平,并且能够下调PGE2和GSK-3β抑制剂SB-216763诱导的VEGF高表达。结论:丹参酮ⅡA通过抑制人肠癌细胞中COX-2的表达,阻止细胞中β-catenin的累积,从而阻断Wnt/β-catenin信号通路,下调VEGF表达,这可能是丹参酮ⅡA抗大肠癌血管新生的作用机制之一。 | 刘宣 王炎 李丹光 周利红 殷佩浩 隋华 范忠泽 李琦 | 2013 | 中华中医药杂志2013，28，1： | 46 |
| 6 | WNT signaling regulates self-renewal and differentiation of prostate cancer cells with stem cell characteristics显示文摘有干细胞特征的前列腺癌症房间被他们在非支持者文化从单个房间形成自我更新的 prostaspheres 的能力在人的前列腺癌症房间线识别。Prostaspheres 展出了增长,区别和茎的异构的表示联系房间的制造者 CD44, ABCG2 和 CD133。有 WNT 禁止者的治疗减少了 prostasphere 尺寸和自强。相反,引起的 Wnt3a 的增加增加了 prostasphere 尺寸和自强,它与原子尾 - catenin 的重要增加被联系,角质素 18, CD133 和 CD44 表示。作为 LNCaP 和 C4-2B 癌症房间快车雄激素受体的一个高比例,我们决定了雄激素受体对手 bicalutamide 的效果。雄激素受体抑制减少了 prostasphere 尺寸和 PSA 的表示,但是没禁止 prostasphere 形成。这些效果与有干细胞特征和放大房间的运输的雄激素依赖者增长的房间的雄激素无关的自强一致。作为发信号的受动器尾 - catenin 能也与雄激素受体联系的正规 WNT,我们为包含在 WNT 和雄激素受体活动之间的平衡的瘤繁殖建议一个模型。那将与干细胞特征和开车运输放大房间增长和区别影响一个癌症房间的自强。在结论,我们提供那项 WNT 活动独立于雄激素受体活动与干细胞特征调整前列腺癌症房间的自强的证据。WNT 发信号的抑制因此有潜力与干细胞特征减少前列腺癌症房间的自强并且改进治疗学的结果。 | Isabelle Bisson David M Prowse | 2009 | Cell Research2009，，6： | 37 |
| 7 | Molecular mechanisms of mesenchymal stem cell differentiation towards osteoblasts显示文摘Bone is a dynamic tissue that is constantly renewed by the coordinated action of two cell types, i.e., the bone-resorbing osteoclasts and the bone-forming osteoblasts. However, in some circumstances, bone regeneration exceeds bone self repair capacities. This is notably often the case after bone fractures, osteolytic bone tumor surgery, or osteonecrosis. In this regard,bone tissue engineering with autologous or allogenic mesenchymal stem cells(MSCs) is been widely developed. MSCs can be isolated from bone marrow or other tissues such as adipose tissue or umbilical cord, and can be implanted in bone defects with or without prior amplification and stimulation. However, the outcome of most pre-clinical studies remains relatively disappointing. A better understanding of the successive steps and molecular mechanisms involved in MSC-osteoblastic differentiation appears to be crucial to optimize MSC-bone therapy. In this review, we first present the important growth factors that stimulate osteoblastogenesis. Then we review the main transcription factors that modulate osteoblast differentiation, and the microRNAs(miRs)that inhibit their expression. Finally, we also discuss articles dealing with the use of these factors and miRs in the development of new bone MSC therapy strategies. We particularly focus on the studies using human MSCs, since significant differences exist between osteoblast differentiation mechanisms in humans and mice for instance. | Maya Fakhry René Buchet David Magne Eva Hamade Bassam Badran | 2013 | World Journal of Stem Cells2013，5，4： | 32 |
| 8 | COX-2/PGE_2激活Wnt/β-catenin信号通路调控人肠癌细胞VEGF表达显示文摘目的探讨环氧化酶2(COX-2)/前列腺素E2(PGE2)是否通过Wnt/β-catenin信号通路调控人肠癌细胞血管内皮生长因子(VEGF)的表达。方法将PGE2或COX-2选择性抑制剂NS-398作用LoVo细胞24h,采用蛋白质印迹法检测COX-2和β-catenin蛋白表达;将PGE2和(或)β-catenin/tcf抑制剂FH-535作用LoVo细胞24h,采用ELISA法检测VEGF表达。以常规培养的LoVo细胞为对照。结果与对照组比较,PGE2能够上调LoVo细胞中COX-2蛋白表达,同时上调β-catenin在细胞总蛋白、细胞浆蛋白和核蛋白中的表达水平(分别是对照组的3.8倍、2.7倍和3.0倍,P均<0.01);COX-2抑制剂能够下调COX-2蛋白表达,同时下调β-catenin在细胞总蛋白、细胞浆蛋白和核蛋白中的表达水平(分别是对照组的0.3倍、0.3倍和0.2倍,P均<0.01)。与对照组比较,PGE2能够上调LoVo细胞VEGF表达水平(是对照组的1.6倍,P<0.01);β-catenin/tcf抑制剂能够下调VEGF表达(是对照组的0.68倍,P<0.01);将PGE2和β-catenin/tcf抑制剂同时作用LoVo细胞后VEGF表达水平与对照组相比差异无统计学意义(P>0.05)。结论 COX-2/PGE2通过上调β-catenin蛋白表达,从而激活Wnt/β-catenin信号通路,上调VEGF表达,这可能是COX-2/PGE2促进大肠癌血管新生的机制之一。 | 刘宣 李丹光 周利红 王炎 殷佩浩 季青 范忠泽 李琦 | 2012 | 第二军医大学学报2012，33，11： | 32 |
| 9 | 杜仲醇提取物诱导骨髓间充质干细胞成骨分化中的Wnt信号途径显示文摘背景:近年来,中药及中药有效部分对骨质疏松的干预和治疗作用的报道较多,但涉及细胞成骨分化调控的信号途径的报道较少。目的:观察杜仲诱导大鼠骨髓间充质干细胞成骨分化过程中Wnt信号途径相关基因表达的变化。方法:将第3代SD大鼠骨髓间充质干细胞,接种到6孔培养板中,每孔1×103个细胞,24h后更换诱导培养基(含体积分数为7.5%胎牛血清的DMEM/F12(1:1)加1/1000浓度的杜仲醇提取物)。阴性对照组仍为正常培养基培养。诱导8h,1d,3d和7d时采用RT-qPCR法测定Wnt信号途径中Fzd和LRP受体系列、β-catenin、核内Wnt调控靶基因系列及Wnt抑制因子(WIF1)等表达变化。结果与结论:与阴性对照组比较,诱导3d后Fzd2表达升高11.86倍,Fzd3升高达到2倍;诱导7d后,Fzd2表达升高5.12倍,Fzd3恢复到正常水平;β-catenin在诱导3d时表达升高达2倍;WIF1在诱导3d和7d后表达显著下降。结果提示Wnt信号途径可能参与了杜仲促骨髓间充质干细胞成骨分化过程。 | 张贤 朱丽华 钱晓伟 谭湘陵 | 2012 | 中国组织工程研究2012，16，45： | 34 |
| 10 | FoxO/Wnt通路在氧化应激介导的骨质疏松中的调控机制显示文摘在衰老机体中,过量的活性氧自由基(ROS)可产生氧化应激(OS),降低骨量和骨质量,诱发骨质疏松。β-catenin与Wnt通路下游的TCF作用可调控骨形成,与FoxO作用可产生抗OS作用,'以衰老和氧化应激为中心'已成为骨质疏松研究的新焦点,抗氧化剂具有防治骨质疏松潜力。 | 杨亚军 崔燎 | 2013 | 中国药理学通报2013，29，1： | 32 |
| 11 | PI3K/Akt信号通路在骨质疏松病理过程中的作用显示文摘磷脂酰肌醇三激酶/蛋白激酶B(PI3K/Akt)信号通路是调节细胞增殖、分化、存活、迁移和代谢过程的最为重要的一个信号通路。越来越多的证据表明,骨组织中的许多信号分子能够选择性激活PI3K/Akt信号通路的相关基因,通过调控成骨细胞和破骨细胞的活动,破坏骨重建过程中骨形成与骨吸收的动态平衡,在骨质疏松的发生和发展中扮演着非常重要的角色。 | 陈亚辉 龚忠勤 崔燎 | 2015 | 中国骨质疏松杂志2015，21，3： | 32 |
| 12 | Wnt信号转导通路在肿瘤中的研究进展显示文摘Wnt信号转导通路具有传递生长刺激信号的作用,与细胞的发育、分化密切相关。Wnt信号转导通路的异常激活,可引起细胞异常增殖及分化而导致肿瘤的发生。另外,其信号转导通路在人类不同肿瘤中的作用是相互交织的,了解该通路在肿瘤发生过程中的转导及调控,有助于为临床诊断提供依据,为早期干预治疗提供方法。 | 王震凯 朱人敏 | 2007 | 医学研究生学报2007，20，12： | 29 |
| 13 | 黄芪丹参颗粒药对干预肾纤维化Wnt/β-catenin信号通路的实验研究显示文摘目的:观察黄芪丹参颗粒药对对肾纤维化信号通路Wnt/β-catenin的影响,并初步明确其量效关系。方法:40只雄性SD大鼠,随机分为5组,即正常组,模型组,黄芪丹参颗粒药对(1∶1)低剂量治疗组,黄芪丹参颗粒药对(1∶1)中剂量治疗组,黄芪丹参颗粒药对高剂量(1∶1)治疗组。除正常组外,其余大鼠均建立单侧输尿管梗阻(UUO)模型。各组给予相应药物治疗,收集尿液检测24 h尿蛋白、α1-微球蛋白(α1-Microglobulin,α1-MG)的含量,光镜观察肾组织病理;Western Blot技术检测肾组织Wnt4和β-catenin蛋白表达。结果:①24 h尿蛋白和α1-MG检测结果,与正常组比较,模型组24 h尿蛋白和α1-MG均明显升高(P<0.05);与模型组比较,各治疗组24 h尿蛋白和α1-MG明显降低(P<0.05);与颗粒低剂量组比较,颗粒中、高剂量组24h尿蛋白均明显降低(P<0.05),各剂量组之间α1-MG差异无显著性。②HE染色结果,各治疗组病理变化较模型组均有明显改善,与颗粒低剂量组比较,颗粒中、高剂量组评分明显减少(P<0.05)。③肾组织Wnt4和β-catenin免疫印迹检测结果,与正常组比较,模型组和各剂量组大鼠肾组织Wnt4和β-catenin具有明显有升高趋势,各治疗组均有不同程度下降,尤以颗粒中、高剂量组下降明显。结论:黄芪丹参(1∶1)颗粒药对可以保护UUO大鼠肾小管功能,一定程度改善UUO大鼠肾脏病理改变,其机制可能与干预Wnt/β-catenin信号通路有关。黄芪丹参颗粒药对可以干预UUO大鼠肾组织中Wnt4、β-catenin的表达,并存在一定的量效关系。 | 付旭 李均 阳小敏 赵任杰 周萍 顾铜 | 2014 | 世界科学技术-中医药现代化2014，，1： | 29 |
| 14 | 鳖甲煎丸对肝细胞癌中Wnt/β-catenin信号通路及抑制基因DKK-1、FrpHe表达的影响显示文摘目的通过研究鳖甲煎丸对肝细胞癌中Wnt信号通路及抑制基因DKK-1、FrpHe表达的影响,探讨其抗肝细胞癌转移侵袭的作用机制与Wnt/β-catenin信号通路的关系。方法 24只Wistar大鼠随机分为3组(8只/组),分别以临床剂量的20倍、10倍的鳖甲煎丸和生理盐水灌胃3 d,3 d后采血,离心,获取血清。分别将3组血清加入DMEM培养液中培养肝癌细胞HepG2,48 h后采用流式细胞术检测细胞中的β-catenin蛋白含量,qRT-PCR法检测DKK-1、FrpHe基因的表达情况,以进一步阐明药物的作用机制与Wnt/β-catenin信号通路的关系。结果流式细胞术结果:高剂量组和中剂量组含药血清均可显著降低细胞中β-catenin蛋白表达,且该作用与药物浓度有关。RT-PCR结果:高剂量组和中剂量组含药血清均可显著下调DKK-1基因的表达,且该作用与药物浓度有关。而高剂量组和中剂量组含药血清对FrpHe基因的表达影响不明显。结论鳖甲煎丸能显著抑制肝细胞癌的生长、粘附和转移,且这种抑制作用与显著降低肝癌细胞中β-catenin蛋白表达、显著下调DKK-1基因的表达,从而阻断Wnt/β-catenin信号通路有关。 | 贺松其 程旸 朱云 范钦 孙海涛 贾文燕 | 2013 | 南方医科大学学报2013，33，1： | 28 |
| 15 | 健脾解毒方通过COX-2-Wnt/β-catenin信号通路抑制裸鼠人结肠癌血管新生显示文摘目的:研究健脾解毒方对裸鼠人结肠癌血管新生的作用及机制。方法:建立人结肠癌HT-29细胞裸鼠皮下移植瘤模型,随机分为5组:对照组(0.9%氯化钠溶液组),健脾解毒方低、中、高剂量组(250、500、1 000mg·kg-1·d-1)和化疗药顺铂组(1mg·kg-1·d-1)。给药第21天,处死各组荷瘤鼠,比较各组肿瘤大小。免疫组化法检测各组瘤体的微血管密度(MVD)、COX-2和β-catenin表达;ELISA测定血清中血管内皮生长因子(VEGF)、血管生成素(Ang-2)和碱性成纤维细胞生长因子(bFGF)的表达。结果:健脾解毒方低、中、高剂量组的瘤重抑制率分别为30.14%、38.01%、40.36%。免疫组化结果显示,对照组、健脾解毒方低、中、高剂量组瘤体MVD计数分别为(56.00±2.65)、(43.00±1.58)、(28.67±2.53)和(23.33±2.08),与对照组比较差异显著(P<0.01)。ELISA结果显示,健脾解毒方能够显著下调裸鼠血清中VEGF、Ang-2和bFGF表达(P<0.01)。同时,健脾解毒方能够显著下调瘤体中COX-2和β-catenin蛋白表达,呈剂量依赖效应。结论:健脾解毒方能抑制人结肠癌皮下移植瘤的生长和血管新生,其机制可能通过COX-2-Wnt/β-catenin信号通路下调VEGF表达有关。 | 刘宣 王炎 隋华 殷佩浩 王一斐 范忠泽 李琦 | 2013 | 中华中医药杂志2013，28，5： | 28 |
| 16 | 黄芪多糖通过Wnt/β-catenin信号通路促进肝癌细胞凋亡研究显示文摘目的探讨黄芪多糖通过Wnt/β-catenin信号通路对人肝癌Hep G2细胞增殖及凋亡的影响。方法四甲基偶氮唑蓝(MTT)法检测Hep G2细胞增殖能力和存活率;Annexin V-FITC/PI双染和Caspase-3活性检测细胞凋亡;荧光素酶实验检测黄芪多糖(100、200 mg/L)处理后Hep G2细胞Wnt/β-catenin通路活性改变;实时荧光定量PCR(qRT-PCR)、Western blotting法检测细胞内的β-catenin、c-myc和CyclinD1表达水平。结果与对照组比较,随着黄芪多糖质量浓度的增加和作用时间的延长,Hep G2细胞存活率显著降低(P<0.05)。与对照组比较,黄芪多糖100、200mg/L组Hep G2细胞凋亡率显著升高(P<0.05);凋亡关键因子Caspase-3的相对活性显著升高(P<0.05),cleaved Caspase-3蛋白水平显著升高,Bcl-2蛋白表达水平显著降低;荧光素酶活性显著降低(P<0.05);β-catenin、c-myc和Cyclin D1 mRNA及蛋白表达水平显著降低(P<0.05、0.01)。结论黄芪多糖通过下调Wnt/β-catenin信号通路抑制凋亡相关基因Bcl-2的表达,促进Hep G2细胞凋亡。 | 吕君 朱鹏飞 刘艳民 曾庆磊 余祖江 | 2018 | 中草药2018，49，21： | 28 |
| 17 | Abnormal β-catenin gene expression with invasiveness of primary hepatocellular carcinoma in China显示文摘AIM To study the abnormal expression of β-catenin gene and its relationship with invasiveness of primary hepatocellular carcinoma among Chinese people.METHODS Thirty-four hepatocellular carcinoma (HCC) specimens and adjacent para-cancerous tissues, 4 normal liver tissues were immunohistochemically stained to study subcellular distribution of β-catenin. Semiquantitive analysis of expression of β-catenin gene exon 3 mRNA was examined by RT-PCR and in situ hybridization. The relationship between expressions of both β-catenin protein, mRNA and clinicopathological characteristics of HCC was also analyzed.RESULTS Immunohistochemistry showed that all normal liver tissues and para-cancerous tissues examined displayed membranous type staining for β-catenin protein,occasionally with weak expression in the cytoplasm.While 21 cases (61.8%) of HCC examined showed accumulated type in cytoplasms or nuclei. The accumuled type Labling Index (LI) of cancer tissue and paracancarous tissue was (59.9 ± 26.3) and (18.3 ± 9.7)respectively (P<0.01). Higher accumulated type LI was closely related with invasiveness of HCC. Results of RTPCR showed the β-catenin gene exon 3 mRNA Expression Index (El) of 34 HCCs was higher than that of paracancerous tissue and normal liver tissue. Using in situ hybridization, the signal corresponding to β-catenin gene exon 3 mRNA was particularly strong in cytoplasm of HCC when compared with those of para-cancerous and normal liver tissues. Over expression of β-catenin exon 3 was also found to be correlated with high metastatic potential of HCC.CONCLUSION Abnormal expression of β-catenin gene may contribute importantly to the invasiveness of HCC among Chinese people. | Maija H Zile | 2001 | World Journal of Gastroenterology2001，7，4： | 22 |
| 18 | Wnt/β-catenin信号通路对人肠癌细胞VEGF表达的调控作用显示文摘背景与目的:血管新生是导致大肠癌向其他脏器组织侵袭、转移的重要原因。血管内皮生长因子(vascular endothelial growth factor,VEGF)是重要的促血管生成因子之一,但其过表达机制尚不清楚。Wnt/β-catenin信号通路在大肠癌发生中存在过度激活,故与大肠癌的发生、发展密切相关。本研究旨在探讨Wnt/β-catenin信号通路对人肠癌VEGF表达的调控作用,揭示大肠癌血管新生的部分机制。方法:分别采用GSK-3β抑制剂SB-216763激活人肠癌HCT-116细胞Wnt/β-catenin信号通路和β-catenin/tcf抑制剂FH-535抑制Wnt/β-catenin信号通路,蛋白质印迹法(Western blot)法检测β-catenin蛋白表达,ELISA法检测细胞培养上清液中VEGF表达。结果:GSK-3β抑制剂SB-216763作用人肠癌HCT-116细胞后,β-catenin在细胞总蛋白、细胞质蛋白和核蛋白中的表达均明显升高,12 h达到最大值,分别是对照组的4.3、3.6和3.7倍(P<0.01);同时,激活Wnt/β-catenin信号通路能够上调人肠癌HCT-116细胞VEGF表达水平,并在24 h时差异最显著,是对照组的1.85倍(P<0.01);而抑制Wnt/β-catenin信号通路能够显著下调VEGF表达,是对照组的0.68倍(P<0.01)。结论:Wnt/β-catenin信号通路能够调控人肠癌细胞VEGF表达。 | 刘宣 王炎 殷佩浩 周利红 朱惠蓉 范忠泽 李琦 | 2012 | 中国癌症杂志2012，22，12： | 21 |
| 19 | Loss of canonical Wnt signaling is involved in the pathogenesis of Alzheimer's disease显示文摘Alzheimer's disease(AD) is the most common form of dementia in the older population, however, the precise cause of the disease is unknown. The neuropathology is characterized by the presence of aggregates formed by amyloid-β(Aβ) peptide and phosphorylated tau; which is accompanied by progressive impairment of memory. Diverse signaling pathways are linked to AD, and among these the Wnt signaling pathway is becoming increasingly relevant, since it plays essential roles in the adult brain. Initially, Wnt signaling activation was proposed as a neuroprotective mechanism against Aβ toxicity. Later, it was reported that it participates in tau phosphorylation and processes of learning and memory. Interestingly, in the last years we demonstrated that Wnt signaling is fundamental in amyloid precursor protein(APP) processing and that Wnt dysfunction results in Aβ production and aggregation in vitro. Recent in vivo studies reported that loss of canonical Wnt signaling exacerbates amyloid deposition in a transgenic(Tg) mouse model of AD. Finally, we showed that inhibition of Wnt signaling in a Tg mouse previously at the appearance of AD signs, resulted in memory loss, tau phosphorylation and Aβ formation and aggregation; indicating that Wnt dysfunction accelerated the onset of AD. More importantly, Wnt signaling loss promoted cognitive impairment, tau phosphorylation and Aβ1–42 production in the hippocampus of wild-type(WT) mice, contributing to the development of an Alzheimer's-like neurophatology. Therefore, in this review we highlight the importance of Wnt/β-catenin signaling dysfunction in the onset of AD and propose that the loss of canonical Wnt signaling is a triggering factor of AD. | Cheril Tapia-Rojas Nibaldo C.Inestrosa | 2018 | Neural Regeneration Research2018，13，10： | 21 |
| 20 | 补肾活血颗粒对去势大鼠骨组织Wnt/β-Catenin通路的影响研究显示文摘目的:探究补肾活血颗粒通过经典Wnt/β-Catenin信号通路防治骨质疏松症(OP)的作用机制。方法:将36只SD大鼠分成模型组、假手术组及补肾活血组,每组12只,模型组及补肾活血组行双侧卵巢切除术、假手术组行假手术处理进行造模,造模成功后各组分别给予0.9%氯化钠溶液、0.9%氯化钠溶液及补肾活血中药灌胃3个月后处死,检测血清雌二醇(E2)、碱性磷酸酶(ALP)、血钙素(BGP),右侧股骨骨盐密度(BMD)和HE染色及腰椎最大承载力,左侧股骨采用RT-PCR检测β-catenin、Runx2、Osx mRNA的表达。结果:补肾活血组与模型组大鼠相比较,血清E2明显上升(P<0.01);骨形成指标ALP、BGP水平明显升高(P<0.05);股骨BMD与腰椎最大承载力均有提高(P<0.05);HE染色观察发现骨小梁稍细,略有变薄,排列较整齐并能够连接成网,密度、面积尚正常,部分区域骨小梁间隙略有增大;β-catenin、Runx2及Osx的mRNA表达均有明显的提高(P<0.01)。结论:激活经典Wnt/β-catenin信号通路是补肾活血颗粒防治骨质疏松症的可能作用机制。 | 许兵 金红婷 刘慧 王萧枫 童培建 肖鲁伟 | 2013 | 中华中医药杂志2013，28，11： | 21 |
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