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Effect of epidermal growth factor on the migration of neural stem cells

Neural Regeneration Research 2006年第6期1卷 502-504页

作者： Faliang Duan Guoping Yang Junwu Wei Jinglei Wu Department of Neurosurgery First Hospital of Wuhan Wuhan 430022 Hubei Province China

BACKGROUND： Recently, researches on neural stem cells （NSCs） are focus on differentiation and migration ot stem cells. How to regulate and control differentiation and migration of NSCs based on human wills is still a hot topic. OBJECTIVE ： To investigate the effect of epidermal growth factor （EGF） on the migration and proliferation of NSCs and analyze duration of the effect. DESIGN ： Contrast study based on cells SETTING ： Department of Neurological Surgery, the First Hospital of Wuhan MATERIALS： Healthy SD rats aged 13-14 embryonic days. EGF （Sigma Company） METHODS： The experiment was carried out in the Animal Laboratory of Experimental Center Affiliated to the First Hospital of Wuhan from October 2004 to July 2006. NSCs selected from embryonic striatum of rats with 13-14 embryonic days were cultured; 7 days later, suspended neural sphere was used to make simple cell suspension and cultured once more. Then, DMEM-F12＋20 μg/L EGF was added into culture medium; 14 days later, the rats were divided into experimental group and control group. Rats in the experimental group were cultured with the same medium mentioned above; however, rats in the control group were cultured with only DMEM-F12. Migration of cells was observed under microscope every day. MAIN OUTCOME MEASURES： NSCs migration in both experimental group and control group RESULTS： Cell spheres in primary culture were NSCs. In addition, 14 days later, proliferation of stem cells were observed remarkably in EGF culture, and size of cell sphere was about that of 100 cells. In experimental group, proliferation of cell sphere was slow down on the 14^th culture day, and apophysis was erupted to neighbor cell sphere. Moreover, NSCs migrated from big cell sphere to small cell sphere during 14-17 culture days, and then, cell migration was disappeared at 17 days after culture. In control group, cell migration was not observed. CONCLUSION： EGF can induce proliferation and migration of NSCs during a special

关键词：表皮生长因子/药理学大鼠 Sprague-Dawley 干细胞/药物作用纹状体/细胞学细胞培养的细胞运动/药物作用大鼠动物女(雌)性妊娠

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BDNF AS对肝癌细胞增殖和迁移能力的影响

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实用肿瘤杂志 2018年第2期33卷 116-121页

作者：郭大伟周品一赵旭鹏初晨江宏伟周勇中国医科大学附属第四医院普外四科辽宁沈阳110032

目的探讨脑源性神经营养因子反义长链非编码RNA(brain-derived neurotrophic factor antisense long noncoding RNA,BDNF AS)对人肝癌细胞增殖和迁移能力的影响。方法采用BDNF AS过表达质粒及空载体瞬时转染肝癌细胞株HepG2和MHCC 97-H... 详细信息

目的探讨脑源性神经营养因子反义长链非编码RNA(brain-derived neurotrophic factor antisense long noncoding RNA,BDNF AS)对人肝癌细胞增殖和迁移能力的影响。方法采用BDNF AS过表达质粒及空载体瞬时转染肝癌细胞株HepG2和MHCC 97-H,采用实时PCR方法检测BDNF AS在肝癌细胞中的表达水平,采用3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)方法检测细胞增殖情况,采用碘化丙啶(propidium iodide,PI)染色流式细胞术检测细胞周期变化,采用划痕实验和transwell小室评价细胞迁移能力的变化。结果 HepG2和MHCC 97-H细胞转染BDNF AS过表达质粒后BDNF AS和mRNA表达均上调(均P<0.01)。转染第4天,细胞增殖均受到抑制(均P<0.05)。转染48 h后,HepG2和MHCC 97-H细胞均出现S期阻滞(均P<0.01),细胞的迁移能力均下降(均P<0.01)。结论 BDNF AS过表达抑制肝癌细胞的增殖和迁移,可能对肝癌细胞的生长运动具有重要的负性调控作用。

关键词：癌,肝细胞/病理学肝肿瘤/病理学脑源性神经营养因子/药理学细胞增殖/药物作用细胞运动/药物作用肿瘤侵润 RNA,信使/生物合成 RNA,信使/遗传学细胞系,肿瘤

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3-溴丙酮酸对人乳头瘤状甲状腺癌TPC-1细胞迁移和侵袭能力的影响

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实用肿瘤杂志 2020年第3期35卷 210-216页

作者：于敬坤陈俊卯孙雅涵何玛莉张琪王长友华北理工大学附属医院普通外科河北唐山063000 华北理工大学医学实验研究中心河北唐山063000

目的观察3-溴丙酮酸对体外人乳头瘤状甲状腺癌TPC-1细胞增殖、迁移和侵袭能力的影响及其相关机制。方法分别用含0、20、40、60、80、100、120、140、160、180和200μmol/L 3-溴丙酮酸的细胞培养液培养TPC-1细胞24 h后,MTT检测细胞增殖... 详细信息

目的观察3-溴丙酮酸对体外人乳头瘤状甲状腺癌TPC-1细胞增殖、迁移和侵袭能力的影响及其相关机制。方法分别用含0、20、40、60、80、100、120、140、160、180和200μmol/L 3-溴丙酮酸的细胞培养液培养TPC-1细胞24 h后,MTT检测细胞增殖活性。含0、100和200μmol/L 3-溴丙酮酸的细胞培养液培养TPC-1细胞24 h或48 h后,划痕实验及transwell实验检测细胞迁移和侵袭能力,Western blot检测基质金属蛋白酶2(matrix metalloproteinase 2,MMP-2)、MMP-9、人源葡萄糖转运蛋白1(glucose transporter 1,Glut1)和Ⅰ型膜型基质金属蛋白酶(membrane-type 1 matrix metalloproteinase,MT1-MMP)的表达水平。结果100、120、140、160、180和200μmol/L 3-溴丙酮酸均抑制TPC-1细胞的增殖活性,呈剂量依赖性(均P<0.01)。3-溴丙酮酸作用于TPC-1细胞24和48 h,随着药物浓度的增高,TPC-1细胞迁移越慢,侵袭细胞越少(均P<0.05)。3-溴丙酮酸作用于TPC-1细胞24和48 h,TPC-1细胞内Glut1、MT1-MMP、MMP-2和MMP-9表达水平均随药物浓度增高而减弱(均P<0.05)。结论3-溴丙酮酸可抑制TPC-1细胞的增殖、迁移及侵袭能力,并可能与下调Glut1、MT1-MMP、MMP-2和MMP-9蛋白表达有关。

关键词：甲状腺肿瘤/病理学腺癌,乳头状/病理学丙酮酸/药理学细胞增殖/药物作用细胞运动/药物作用肿瘤侵润/药物作用葡萄糖转运蛋白质类,易化性基质金属蛋白酶-9 信号传导肿瘤细胞,培养的

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N-(3-三氟甲基苯基)维甲酰胺对人肺腺癌A549细胞迁移能力的影响及其可能机制

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安徽医科大学学报 2011年第5期46卷 439-442页

作者：王银凤程英桂淑玉陈飞虎周青汪渊安徽医科大学第一附属医院呼吸内科合肥230022 安徽医科大学分子生物学实验室和安徽省重要遗传疾病基因资源利用重点实验室合肥230032 安徽医科大学药学院合肥230032

目的研究全反式维甲酸(ATRA)衍生物[N-(3-三氟甲基苯基)维甲酰胺,NTFMP]对人肺腺癌A549细胞株迁移能力的影响及其可能机制。方法应用细胞迁移实验分析NTFMP对A549细胞迁移能力的影响,Western blot检测NTFMP对肌球蛋白轻链激酶(MLCK)的... 详细信息

目的研究全反式维甲酸(ATRA)衍生物[N-(3-三氟甲基苯基)维甲酰胺,NTFMP]对人肺腺癌A549细胞株迁移能力的影响及其可能机制。方法应用细胞迁移实验分析NTFMP对A549细胞迁移能力的影响,Western blot检测NTFMP对肌球蛋白轻链激酶(MLCK)的表达和肌球蛋白轻链(MLC)磷酸化的影响。结果 1、7.5 mg/L NTFMP均可抑制A549细胞的迁移,迁移距离随药物浓度的增加而明显下降,7.5 mg/L NTFMP显著抑制MLCK的表达和MLC磷酸化,而对MLC蛋白表达无明显作用。运用双变量相关分析,发现A549细胞的迁移与细胞内MLCK含量和MLC磷酸化程度呈正相关。结论 NTFMP对A549细胞迁移有抑制作用,其机制可能与MLCK表达和MLC磷酸化下调有关。

关键词：肺肿瘤细胞运动/药物作用维甲酸/类似物和衍生物肌球蛋白轻链激酶

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Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第14期275卷 10661-10672页

作者： Rousseau, S Houle, F Kotanides, H Witte, L Waltenberger, J Landry, J Huot, J Univ Laval Hotel Dieu Quebec Ctr Rech Cancerol Quebec City PQ G1R 2J6 Canada Univ Ulm Med Ctr Dept Internal Med 2 D-89081 Ulm Germany ImClone Syst Inc Dept Mol & Cell Biol New York NY 10014 USA

In endothelial cells, vascular endothelial growth factor (VEGF) induces an accumulation of stress fibers associated with new actin polymerization and rapid formation of focal adhesions at the ventral surface of the cells. This cytoskeletal reorganization results in an intense motogenic activity. Using porcine endothelial cells expressing one or the other type of the VEGF receptors, VEGFR1 or VEGFR2, or human umbilical vein endothelial cells pretreated with a VEGFR2 neutralizing antibody, we show that VEGFR2 is responsible for VEGF-induced activation of the stress-activated protein kinase-2/p38 (SAPK2/p38), phosphorylation of focal adhesion kinase (FAK), and enhanced migratory activity. Activation of SAPK2/p38 triggered actin polymerization whereas FAX, which was phosphorylated independently of SAPK2/p38, initiated assembly of focal adhesions. Both processes contributed to the formation of stress fibers. Geldanamycin, an inhibitor of HSP90 blocked tyrosine phosphorylation of FAK, assembly of focal adhesions, actin reorganization, and cell, migration, all of which were reversed by overexpressing HSP90. We conclude that VEGFR2 mediates the physiological effect of VEGF on cell migration and that two independent pathways downstream of VEGFR2 regulate actin-based motility. One pathway involves SAPK2/p38 and leads to enhanced actin polymerization activity. The other involves HSP90 as a permissive signal transduction factor implicated in FAK phosphorylation and assembly of focal adhesions.

关键词：肌动蛋白类/生理学抗体/药理学苯醌类钙-钙调素依赖性蛋白激酶类/代谢细胞黏附细胞运动/药物作用细胞运动/生理学细胞培养的细胞支架蛋白质类/生理学内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶激活黏着斑激酶1 黏着斑蛋白酪氨酸激酶类 HSP90热休克蛋白质类/拮抗剂和抑制剂 HSP90热休克蛋白质类/遗传学 HSP90热休克蛋白质类/生理学内酰胺类大环淋巴因子/药理学丝裂原激活蛋白激酶类桩蛋白磷蛋白类/生理学磷酰化蛋白酪氨酸激酶类/拮抗剂和抑制剂蛋白酪氨酸激酶类/代谢原癌基因蛋白质类/生理学醌类/药理学受体蛋白质酪氨酸激酶类/免疫学受体蛋白质酪氨酸激酶类/生理学受体生长因子/免疫学受体生长因子/生理学受体血管内皮生长因子脐静脉血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类纽蛋白/生理学 p38丝裂原活化蛋白激酶类人类

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Genomic and functional changes induced by the activation of the peripheral cannabinoid receptor CB2 in the promyelocytic cells HL-60 -: Possible involvement of the CB2 receptor in cell differentiation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第21期275卷 15621-15628页

作者： Derocq, JM Jbilo, O Bouaboula, M Ségui, M Clère, C Casellas, P Sanofi Synthelabo F-34184 Montpellier 04 France

The function of the peripheral cannabinoid receptor (CB2), which is mainly expressed on hematopoietic cells, remains an enigma. In an attempt to decipher its role, we used Affymetrix(TM) DNA chips to investigate the gene expression profile of the promyelocytic cells HL-60 transfected with the CB2 receptor and activated with the cannabinoid agonist CP 55,940, Agonist exposure of these cells led to an activation of a mitogen-activated protein kinase cascade and a receptor desensitization, indicating a functional coupling of the transfected receptors. At the genomic level, activation of the CB2 receptors induced an up-regulation of nine genes involved in cytokine synthesis, regulation of transcription, and cell differentiation. A majority of them are under the control of the transcription factor NF-kappa B, whose nuclear translocation was demonstrated. Many features of the transcriptional events, reported here for the first time, appeared to be related to an activation of a cell differentiation program, suggesting that CB2 receptors could play a role in the initialization of cell maturation. Moreover, we showed that CB2-activated wild-type HL-60 cells developed properties usually found in host defense effector cells such as an enhanced release of chemotactic cytokines and an increased motility, characteristic of more mature cells of the granulocytic-monocytic lineage.

关键词：冰片烷类/药理学大麻酚类/药理学细胞分化/药物作用细胞分化/遗传学细胞运动/药物作用环己醇类/药理学细胞因子类/遗传学细胞因子类/代谢基因表达调控/药物作用 HL-60细胞丝裂原激活蛋白激酶类/代谢 NF-κB/遗传学 NF-κB/代谢寡核苷酸序列分析磷酰化/药物作用吡唑类/药理学 RNA 信使/代谢受体大麻酚受体药物/激动剂受体药物/代谢转染人类

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A peptide representing the carboxyl-terminal tail of the met receptor inhibits kinase activity and invasive growth

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第41期274卷 29274-29281页

作者： Bardelli, A Longati, P Williams, TA Benvenuti, S Comoglio, PM Univ Turin Sch Med Inst Canc Res Treatment I-10060 Candiolo Italy

Interaction of the hepatocyte growth factor (HGF) with its receptor, the Met tyrosine kinase, results in invasive growth, a genetic program essential to embryonic development and implicated in tumor metastasis. Met-mediated invasive growth requires autophosphorylation of the receptor on tyrosines located in the kinase activation loop (Tyr(1234)-Tyr(1235)) and in the carboxyl-terminal tail (Tyr(1349)-Tyr(1356)). We report that peptides derived from the Met receptor tail, but not from the activation loop, bind the receptor and inhibit the kinase activity in vitro. Cell delivery of the tail receptor peptide impairs HGF-dependent Met phosphorylation and downstream signaling. In normal and transformed epithelial cells, the tail receptor peptide inhibits HGF-mediated invasive growth, as measured by cell migration, invasiveness, and branched morphogenesis. The Met tail peptide inhibits the closely related Ron receptor but does not significantly affect the epidermal growth factor, platelet-derived growth factor, or vascular endothelial growth factor receptor activities. These experiments show that carboxyl-terminal sequences impair the catalytic properties of the Met receptor, thus suggesting that in the resting state the nonphosphorylated tail acts as an intramolecular modulator. Furthermore, they provide a strategy to selectively target the MET proto-oncogene by using small, cell-permeable, peptide derivatives.

关键词：衔接蛋白质类信号转导氨基酸序列 COS细胞细胞分裂/药物作用细胞膜通透性细胞运动/药物作用荧光抗体技术肝细胞生长因子/代谢丝裂原激活蛋白激酶类/代谢分子序列数据肿瘤侵润肽碎片/化学肽碎片/药理学磷蛋白类/代谢磷酰化蛋白质结合原癌基因蛋白质c-met/拮抗剂和抑制剂原癌基因蛋白质c-met/化学受体蛋白质酪氨酸激酶类/代谢信号传导肿瘤细胞培养的动物人类

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CORTICOSTEROID INHIBITION OF CHEMOTACTIC LYMPHOKINE PRODUCTION BY T AND B LYMPHOCYTES

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ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1975年第JUN13期256卷 375-385页

作者： WAHL, SM NIDR HUMORAL IMMUN SECT LAB MICROBIOL & IMMUNOL BETHESDA MD 20014 USA

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Chondrocyte translocation response to direct current electric fields

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JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME 2000年第3期122卷 261-267页

作者： Chao, PHG Roy, R Mauck, RL Liu, W Valhmu, WB Hung, CT Columbia Univ Dept Biomed Engn Cellular Engn Lab New York NY 10027 USA Columbia Univ Dept Orthopaed Surg Orthopaed Res Lab New York NY 10032 USA

Using a custom galvanotaxis chamber and time-lapse digital video microscopy, we report the novel observation that cultured chondrocytes exhibit cathodal migration when subjected to applied direct current (DC) electric fields as low as 0.8 V/cm. The response was dose-dependent for field strengths greater than 4 V/cm. Cell migration appeared to be an active process with extension of cytoplasmic processes in the direction of movement. In some cells, field application for greater than an hour induced elongation of initially round cells accompanied by perpendicular alignment of the long axis with respect to the applied field. Antagonists of the inositol phospholipid pathway, U-73122 and neomycin, were able to inhibit cathodal migration. Cell migration toward the cathode did nor require the presence of serum during field application. However, the directed velocity was nearly threefold greater in studies performed with serum. Studies performed at physiologic temperatures (similar to 37 degreesC) revealed a twofold enhancement in migration speed compared to similar studies at room temperature (similar to 25 degreesC). Findings from the present study may help to elucidate basic mechanisms that mediate chondrocyte migration and substrate attachment. Since chondrocyte migration has been implicated in cartilage healing, the ability to direct chondrocyte movement has the potential to impact strategies for addressing cartilage healing/repair and for development of cartilage substitutes.

关键词：细胞运动/药物作用细胞运动/生理学细胞培养的/药物作用细胞培养的/生理学软骨细胞/药物作用软骨细胞/生理学电刺激雌烯类显微镜检查电视新霉素/药理学磷酸二酯酶抑制剂/药理学吡咯烷酮类动物牛

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Deposition of laminin 5 by keratinocytes regulates integrin adhesion and signaling

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第41期275卷 31896-31907页

作者： Nguyen, BP Gil, SG Carter, WG Fred Hutchinson Canc Res Ctr Seattle WA 98109 USA Univ Washington Dept Pathobiol Seattle WA 98195 USA

Deposition of laminin 5 over exposed dermal collagen in epidermal wounds is an early event in repair of the basement membrane. We report that deposition of laminin 5 onto collagen switches adhesion and signaling from collagen-dependent to laminin 5-dependent, Ligation of laminin 5 by integrin alpha(6)beta(4) activates phosphoinositide S-OH-kinase (PI3K) signaling. This activation allows for adhesion and spreading via integrin alpha(3)beta(1) on laminin 5 independent of RhoGTPase, a regulator of actin stress fibers. In contrast, adhesion and spreading on collagen via alpha(2)beta(1) is Rho-dependent and is inhibited by toxin B, a Rho inhibitor. Deposition of laminin 5 and ligation of alpha(6)beta(4) increases PI3K-dependent production of phosphoinositide di- and triphosphates, PI3K activity, and phosphorylation of downstream target protein c-Jun NH3-terminal kinase, Conversely, blocking laminin 5-deposition with brefeldin A, an inhibitor of vesicle transport, or with anti-laminin 5 monoclonal antibodies abolishes the PI3K-dependent spreading mediated by alpha(3)beta(1) and phosphorylation of c-Jun NH2-terminal kinase. Studies with keratinocytes lacking alpha(6)beta(4) or laminin 5 confirm that deposition of laminin 5 and ligation by alpha(6)beta(4) are required for PI3K-dependent spreading via alpha(3)beta(1). We suggest that deposition of laminin 5 onto the collagen substratum, as in wound repair, enables human foreskin keratinocytes to interact via alpha(6)beta(4) and to switch from a RhoGTPase-dependent adhesion on collagen to a PI3K-dependent adhesion and spreading mediated by integrin alpha(3)beta(1) on laminin 5.

关键词：氨基酸序列雄二烯类/药理学细胞黏附/药物作用细胞黏附分子/化学细胞黏附分子/代谢细胞运动/药物作用细胞大小/药物作用细胞培养的胶原/代谢表皮松解大疱性/代谢脱叶素类/药理学黏着斑激酶1 黏着斑蛋白酪氨酸激酶类焦点黏着/药物作用肝素/代谢整合素类/代谢 JNK丝裂原活化蛋白激酶类角蛋白细胞/细胞学角蛋白细胞/药物作用角蛋白细胞/酶学角蛋白细胞/代谢丝裂原激活蛋白激酶类/代谢分子序列数据磷脂酰肌醇类/代谢磷酰化蛋白酪氨酸激酶类/代谢信号传导/药物作用伤口愈合 ρGTP结合蛋白质类/拮抗剂和抑制剂 ρGTP结合蛋白质类/代谢人类

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