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作者：黄国平同济大学

学位级别：硕士

目的通过检测人大肠癌淋巴结微转移和癌旁微淋巴管密度与癌组织淋巴管生成因子VEGF-C、VEGF-D、VEGFR-3的表达，以及与患者临床病理参数和预后的相关性分析，探讨大肠癌淋巴结微转移与淋巴管生成的相关机制。方法应用CEA、CK20免疫组化... 详细信息

目的通过检测人大肠癌淋巴结微转移和癌旁微淋巴管密度与癌组织淋巴管生成因子VEGF-C、VEGF-D、VEGFR-3的表达，以及与患者临床病理参数和预后的相关性分析，探讨大肠癌淋巴结微转移与淋巴管生成的相关机制。方法应用CEA、CK20免疫组化检测35例Dukes B期大肠癌淋巴结微转移情况，5’-Nase-酶组织化学技术对80例大肠癌癌旁组织进行淋巴管染色，光镜下测定癌旁组织微淋巴管密度;应用免疫组化检测经病理确诊的80例大肠癌组织标本的VEGF-C、VEGF-D、VEGFR-3蛋白表达;应用RT-PCR方法检测30例新鲜大肠癌组织标本VEGF-C mRNA、VEGF-D mRNA、VEGFR-3 mRNA的表达;分析大肠癌淋巴结微转移与大肠癌淋巴管生成因子之间的关系及其与癌旁微淋巴管密度相关性;并收集、记录、分析大肠癌Dukes分期、组织学类型、分化程度、淋巴结转移等患者临床病理参数及随访术后生存情况。结果①35例Dukes B期大肠癌淋巴结(共207枚)，CEA检测25．71％(9／35)病例和9．17％(19／207)淋巴结存在微转移，CK20检测28．57％(10／35)病例和11．11％(23／207)淋巴结存在微转移。②在80例大肠癌标本中，癌旁微淋巴管密度为9．76±2．85／视野。癌旁微淋巴管密度与淋巴转移、肝肺转移、Dukes分期、分化程度、预后相关。③80例大肠癌标本中，39例(48．75％)VEGF-C染色阳性，VEGF-C mRNA的表达与VEGF-C蛋白的表达基本一致，VEGF-C的表达与淋巴转移、Dukes分期、预后相关，多变量分析显示VEGF-C是大肠癌患者一个独立的预后因素。④80例大肠癌标本中，45例(56．25％)VEGF-D染色阳性，VEGF-D mRNA的表达与VEGF-D蛋白的表达基本一致，VEGF-D的表达与淋巴转移、Dukes分期相关。⑤80例大肠癌标本中，31例(38．75％)VEGFR-3染色阳性，VEGFR-3 mRNA的表达与VEGFR-3蛋白的表达基本一致，VEGFR-3的表达与淋巴转移、Dukes分期、预后相关。⑥大肠癌癌旁微淋巴管密度与VEGF-C、VEGF-D、VEGFR-3的表达呈正相关。⑦VEGFR-3的表达与VEGF-C、VEGF-D之间均存在相关性，VEGF-C的表达与VEGF-D无相关性。⑧35例Dukes B期大肠癌淋巴结10例微转移检测阳性，阳性组癌旁微淋巴管密度、VEGF-C、VEGFR-3表达与阴性组有显著性差异，VEGF-D表达无明显差异。结论①CEA、CK20免疫组化方法可检出大肠癌淋巴结微转移，对大肠癌的分期和预后判断具有指导意义，其中以CK20具有较高的特异性和敏感性。②在人大肠癌中，VEGF-C、VEGF-D、VEGFR-3表达、癌旁微淋巴管密度明显升高，与淋巴结转移、预后密切相关，多变量分析显示VEGF-C表达是大肠癌患者一个独立的预后因素。VEGF-C、VEGF-D／VEGFR-3信号传导机制促进淋巴管生成，导致癌旁微淋巴管密度升高。③大肠癌淋巴管生成与淋巴结转移、微转移密切相关，促进大肠癌淋巴转移。

关键词：结肠直肠肿瘤淋巴结微转移淋巴管生成血管内皮生长因子C 血管内皮生长因子D 血管内皮生长因子受体3 微淋巴管密度

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肝细胞癌中VEGF-C、VEGFR-3和podoplanin的表达及其与淋巴道转移关系的研究

肝细胞癌中VEGF-C、VEGFR-3和podoplanin的表达及其与淋巴道转移...

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作者：李天满桂林医学院

学位级别：硕士

目的肝细胞肝癌(hepatocellular carcinoma,HCC)是世界范围内最常见的恶性肿瘤之一,居我国癌症死亡的第三位。淋巴道转移是影响肝细胞肝癌(HCC)临床预后的一个重要的决定因素,但是关于肝细胞癌控制淋巴管生成机制知之甚少。在多种动物... 详细信息

目的肝细胞肝癌(hepatocellular carcinoma,HCC)是世界范围内最常见的恶性肿瘤之一,居我国癌症死亡的第三位。淋巴道转移是影响肝细胞肝癌(HCC)临床预后的一个重要的决定因素,但是关于肝细胞癌控制淋巴管生成机制知之甚少。在多种动物模型中证实血管内皮生长因子C(vascular endothelial growth factor C ,VEGF-C)能促进肿瘤淋巴管生成和肿瘤细胞的淋巴结转移及远处转移。Podoplanin是一种相对分子质量为38×103的I型跨膜糖蛋白,是淋巴管内皮细胞的特异性标志物。本文探讨肝细胞癌癌组织中血管内皮生长因子C和血管内皮生长因子受体3(vascular endothelial growth factor receptor 3,VEGFR-3)的表达及其在肝细胞癌进展中的作用。观察淋巴管内皮细胞podoplanin的表达,为研究肝细胞癌淋巴道转移的分子机制提供形态学依据。方法1、取本院2002年4月至2008年11月行手术切除肿瘤和肝外淋巴结并经病理学证实的石蜡包埋的肝细胞肝癌病理标本56例。根据病理学结果将其分为淋巴结转移组和非淋巴结转移组。 2、将病理切片应用即用型二步法(非生物素)免疫组化检测试剂方法检测标本中VEGF-C、VEGFR-3及podoplanin的蛋白表达,检测癌组织中微淋巴管密度(Lymphatic micro-vessel density, LMVD)。结果VEGF-C和VEGFR-3主要表达于肝细胞癌癌细胞胞浆内,肝细胞癌癌组织中VEGF-C和VEGFR-3表达的阳性率明显高于正常肝组织(P<0.01)。肝细胞癌组织中血管内皮细胞podoplanin不染色,淋巴管内皮细胞podoplanin阳性表达,经计数微淋巴管数量,癌组织和癌旁肝组织LMVD明显高于正常肝组织(P<0.01)。结论1、肝细胞癌癌组织中VEGF-C的表达明显增高,推测可能通过与VEGFR-3的结合促进肝细胞癌组织中淋巴管的生成。 2、Podoplanin可选择性的表达在肝细胞癌组织淋巴管内皮上,能明确的区分血管及淋巴管成分,可作为一个淋巴管内皮细胞较特异的标记物。 3、LMVD在肝细胞癌组织中的表达明显增高,及淋巴管数量的增加可能与肝细胞癌的淋巴转移有关。

关键词：肝细胞癌血管内皮生长因子C 血管内皮生长因子受体3 podoplanin 淋巴管微淋巴管密度

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VEGF-A与卵巢癌淋巴管和血管生成及淋巴结转移的关系研究

VEGF-A与卵巢癌淋巴管和血管生成及淋巴结转移的关系研究

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作者：邱敏第三军医大学

学位级别：硕士

目的: 1、探讨卵巢癌组织中是否存在血管内皮生长因子(VEGF-A)的表达或表达上调。2、探讨VEGF-A 与卵巢癌中微血管密度(MVD)、淋巴管密度(LVD)及淋巴结转移的关系。旨在探讨VEGF-A 与卵巢癌淋巴管和血管生成的关系。方法: 1、用免疫组... 详细信息

目的: 1、探讨卵巢癌组织中是否存在血管内皮生长因子(VEGF-A)的表达或表达上调。 2、探讨VEGF-A 与卵巢癌中微血管密度(MVD)、淋巴管密度(LVD)及淋巴结转移的关系。旨在探讨VEGF-A 与卵巢癌淋巴管和血管生成的关系。方法: 1、用免疫组化的方法检测VEGF-A 在42 例良性上皮性卵巢肿瘤组织,20 例交界性上皮性卵巢肿瘤组织和59 例卵巢癌组织中的蛋白表达。 2、用CD34 标记血管,VEGFR-3(vascular endothelial growth factor receptor)标记淋巴管,进行微血管和淋巴管的计数,分析VEGF-A 与MVD 及LVD 的相关性。并分析VEGF-A 与淋巴结转移、FIGO 分期、腹膜转移、组织学类型、年龄及远处转移等临床病理指标之间的关系。 3、联合MVD 及LVD 分析其与临床病理指标之间的关系。 4、利用逆转录-聚合酶链反应(reverse transcriptase polymerase chain reaction, RT-PCR)技术检测比较VEGF-AmRNA 在22 例良性上皮性卵巢肿瘤组织,31 例卵巢癌组织中的表达水平,以凝胶成像系统对结果进行比较分析。 5、结合临床病理资料分析VEGF-AmRNA 与淋巴管密度及淋巴结转移的关系。结果: 1、VEGF-A 阳性染色物为棕黄色细颗粒,主要定位于肿瘤细胞的胞浆及部分基质血管内皮内,其阳性细胞呈局灶性或弥漫性分布。在恶性、交界性和良性卵巢肿瘤组织中皆有VEGF-A 蛋白的表达,但是恶性、交界性和良性卵巢肿瘤组织中VEGF-A蛋白阳性表达率从高至低,三者比较差异均有统计学意义(均为P<0.05)。 2、VEGF-A 阳性组的MVD 与阴性组的MVD 比较有显著性差异(P<0.01)。VEGF-A 阳性组的LVD 与阴性组的LVD 比较有显著性差异(P<0.05)。VEGF-A 的表达与LVD 及MVD 显著正相关。VEGF-A 与淋巴结转移、FIGO 分期及腹膜转移显著相关(分别为P<0.01,P<0.01 及P<0.05)。

关键词：血管内皮生长因子A 免疫组织化学淋巴管密度血管密度卵巢癌逆转录-聚合酶链反应血管内皮生长因子受体3

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Vascular endothelial growth factor-C stimulates the migration and proliferation of Kaposi's sarcoma cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第39期274卷 27617-27622页

作者： Marchiò, S Primo, L Pagano, M Palestro, G Albini, A Veikkola, T Cascone, I Alitalo, K Bussolino, F Univ Turin Sch Med Dept Genet Biol & Biochem Inst Canc Res & Treatment I-10060 Candiolo Italy Univ Turin Sch Med Dept Biomed Sci & Oncol I-10100 Turin Italy Natl Inst Canc Res I-16100 Genoa Italy Ctr Adv Biotechnol I-16100 Genoa Italy Univ Helsinki Haartman Inst Mol Canc Biol Lab SF-00014 Helsinki Finland

Recent evidence suggesting vascular endothelial growth factor-C (VEGF-C), which is a regulator of lymphatic and vascular endothelial development, raised the question whether this molecule could be involved in Kaposi's sarcoma (KS), a strongly angiogenic and inflammatory tumor often associated with infection by human immunodeficiency virus-1. This disease is characterized by the presence of a core constituted of three main populations of "spindle" cells, having the features of lymphatic/vascular endothelial cells, macrophagic/ dendritic cells, and of a mixed macrophage endothelial phenotype. In this study we evaluated the biological response of KS cells to VEGF-C, using an immortal cell line derived from a KS lesion (KS IMM), which retains most features of the parental tumor and can induce KS-like sarcomas when injected subcutaneously in nude mice. We show that VEGFR-3, the specific receptor for VEGF-C, is expressed by KS IMM cells grown in vitro and in vivo. In vitro, VEGF-C induces the tyrosine phosphorylation of VEGFR-2, a receptor also for VEGF-A, as well as that of VEGFR-3. The activation of these two receptors in KS IMM cells is followed by a dose-responsive mitogenic and motogenic response. The stimulation of KS IMM cells with a mutant VEGF-C unable to bind and activate VEFGR-2 resulted in no proliferative response and in a weak motogenic stimulation, suggesting that VEGFR-2 is essential in transducing a proliferative signal and cooperates with VEGFR-3 in inducing cell migration. Our data add new insights on the pathogenesis of KS, suggesting that the involvement of endothelial growth factors may not only determine KS-associated angiogenesis, but also play a critical role in controlling KS cell growth and/or migration and invasion.

关键词：细胞分裂/药物作用细胞培养的趋化作用/药物作用内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学小鼠裸诱变定点磷酰化受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/生理学受体细胞表面/遗传学受体细胞表面/生理学重组蛋白质类/药理学肉瘤卡波西/病理学肉瘤卡波西/病理生理学移植异种肿瘤细胞培养的酪氨酸脐静脉血管内皮生长因子C 血管内皮生长因子受体3 动物人类小鼠

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Polarized vascular endothelial growth factor secretion by human retinal pigment epithelium and localization of vascular endothelial growth factor receptors on the inner choriocapillaris - Evidence for a trophic paracrine relation

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AMERICAN JOURNAL OF PATHOLOGY 1999年第2期155卷 421-428页

作者： Blaauwgeers, HGT Hotkamp, BW Rutten, H Witmer, AN Koolwijk, P Partanen, TA Alitalo, K Kroon, ME Kijlstra, A van Hinsbergh, VWM Schlingemann, RO Univ Amsterdam Acad Med Ctr Dept Ophthalmol NL-1100 DD Amsterdam Netherlands TNO IVVO Gaubius Lab NL-2300 AK Leiden Netherlands Univ Helsinki Haartman Inst Dept Pathol Helsinki Finland Netherlands Ophthalm Res Inst Dept Ophthalmoimmunol NL-1100 AC Amsterdam Netherlands

The retinal pigment epithelium (RPE) maintains the choriocapillaris (CC) in the normal eye and is involved in the pathogenesis of choroidal neovascularization in age-related macular degeneration. Vascular endothelial growth factor-A (VEGF) is produced by differentiated human RPE cells in vitro and in vitro and may be involved in paracrine signaling between the RPE and the CC. We investigated whether there is a polarized secretion of VEGF by RPE cells in vitro. Also, the localization of VEGF receptors in the human retina was investigated. we observed that highly differentiated human RPE cells, cultured on transwell filters in. normoxic conditions, produced two- to sevenfold more VEGF toward their basolateral side as compared to the apical side. In hypoxic conditions, VEGF-A secretion increased to the basal side only, resulting in a three- to 10-fold higher basolateral secretion. By immunohistochemistry in 50 human eyes and in two cynomolgus monkey eyes, KDR (VEGFR-2) and flt-4 (VEGFR-3) were preferentially localized at the side of the CC endothelium facing the RPE cell layer, whereas flt-1 (VEGFR-1) was found on the inner CC and on other choroidal vessels. Our results indicate that RPE secretes VEGF toward its basal side where its receptor KDR is located on the adjacent CC endothelium, suggesting a role of VEGF in a paracrine relation, possibly in cooperation with flt-4 and its ligand, This can explain the known trophic function of the RPE in the maintenance of the CC and its fenestrated permeable phenotype and points to a role for VEGF in normal eye functioning. Up-regulated basolateral VEGF secretion by RPE in hypoxia or loss of polarity of VEGF production may play a role in the pathogenesis of choroidal neovascularization.

关键词：抗体单克隆/分析细胞低氧细胞系细胞培养的脉络膜/解剖学和组织学脉络膜/血液供给脉络膜/代谢内皮生长因子/分泌上皮/解剖学和组织学免疫组织化学淋巴因子/分泌成束猴/解剖学和组织学旁分泌细胞细胞间通讯色素上皮眼/分泌原癌基因蛋白质类/分析受体蛋白质酪氨酸激酶类/分析受体细胞表面/分析受体生长因子/分析受体血管内皮生长因子视网膜/解剖学和组织学视网膜/代谢血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子受体3 血管内皮生长因子类青少年成年人动物儿童人类

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c-fos-induced growth factor/vascular endothelial growth factor D induces angiogenesis in vivo and in vitro

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第17期96卷 9671-9676页

作者： Marconcini, L Marchio, S Morbidelli, L Cartocci, E Albini, A Ziche, M Bussolino, F Oliviero, S Univ Siena Dipartimento Biol Mol I-53100 Siena Italy Univ Turin Dipartimento Genet Biol & Chim Med I-10060 Candiolo Italy Inst Canc Res & Treatment I-10060 Candiolo Italy Univ Siena Ist Sci Farmaceut I-53100 Siena Italy Univ Florence Dipartimento Farmacol I-50121 Florence Italy Ist Nazl Ric Canc I-16100 Genoa Italy Ctr Biotecnol Avanzate I-16100 Genoa Italy

c-fos-induced growth factor/vascular endothelial growth factor D (Figf/Vegf-D) is a secreted factor of the VEGF family that binds to the vessel and lymphatic receptors VEGFR-2 and VEGFR-3, Here,ve report that Figf/Vegf-D is a potent angiogenic factor in rabbit cornea in vivo in a dose-dependent manner. In vitro Figf/Vegf-D induces tyrosine phosphorylation of VEGFR-2 and VEGFR-3 in primary human umbilical cord vein endothelial cells (HUVECs) and in an immortal cell line derived from Kaposi's sarcoma lesion (KS-IMM). The treatment of HUVECs with Figf/Vegf-D induces dose-dependent cell growth. Figf/VEGF-D also induces HUVEC elongation and branching to form an extensive network of capillary-like cords in three-dimensional matrix. In KS-IMM cells Figf/Vegf-D treatment results in dose-dependent mitogenic and motogenic activities. Taken together with the previous observations that Figf/Vegf-D expression is under the control of the nuclear oncogene c-fos, our data uncover a link between a nuclear oncogene and angiogenesis, suggesting that Figf/Vegf-D may play a critical role in tumor cell growth and invasion.

关键词： CHO细胞细胞分裂/药物作用细胞系趋化作用/药物作用角膜/血液供给仓鼠亚科内皮生长因子/药理学内皮血管/药物作用内皮血管/代谢新生血管化生理性/药物作用磷酰化原癌基因蛋白质c-fos/药理学受体蛋白质酪氨酸激酶类/代谢受体细胞表面/代谢受体生长因子/代谢受体血管内皮生长因子酪氨酸/代谢血管内皮生长因子D 血管内皮生长因子受体3 动物人类小鼠兔

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Angiosarcomas express mixed endothelial phenotypes of blood and lymphatic capillaries -: Podoplanin as a specific marker for lymphatic endothelium

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AMERICAN JOURNAL OF PATHOLOGY 1999年第2期154卷 385-394页

作者： Breiteneder-Geleff, S Soleiman, A Kowalski, H Horvat, R Amann, G Kriehuber, E Diem, K Weninger, W Tschachler, E Alitalo, K Kerjaschki, D Univ Vienna Dept Clin Pathol Vienna Austria Univ Vienna Dept Dermatol Div Immunol Allergy & Infect Dis Vienna Austria Univ Vienna Dept Internal Med 3 Div Nephrol & Dialysis Vienna Austria Univ Helsinki Haartman Inst Mol Canc Biol Lab Dept Pathol Helsinki Finland

Angiosarcomas apparently derive from blood vessel endothelial cells;however, occasionally their histological features suggest mixed origin from blood and lymphatic endothelia. In the absence of specific positive markers for lymphatic endothelia the precise distinction between these components has not been possible, Here we provide evidence by light and electron microscopic immunohistochemistry that podoplanin, a similar to 38-kd membrane glycoprotein of podocytes, is specifically expressed in the endothelium of lymphatic capillaries, but not in the blood vasculature, In normal skin and kidney, podoplanin colocalized with vascular endothelial growth factor receptor-3, the only other lymphatic marker presently available. Complementary immunostaining of blood vessels was obtained with established endothelial markers (CD31, CD34, factor VIII-related antigen, and Ulex europaeus I lectin) as well as podocalyxin, another podocytic protein that is also localized in endothelia of blood vessels. Podoplanin specifically immunolabeled endothelia of benign tumorous lesions of undisputed lymphatic origin (lymphangiomas, hygromas) and was detected there as a 38-kd protein by immunoblotting, As paradigms of malignant vascular tumors, poorly differentiated (G3) common angiosarcomas (n = 8), epitheloid angiosarcomas (n = 3), and intestinal Kaposi's sarcomas (n = 5) were examined for their podoplanin content in relation to conventional endothelial markers. The relative number of tumor cells expressing podoplanin was estimated and, although the number of cases in this preliminary study was limited to 16, an apparent spectrum of podoplanin expression emerged that can be divided into a low-expression group in which 0-10% of tumor cells contained podoplanin, a moderate-expression group with 30-60% and a high-expression group with 70-100%. Ten of eleven angiosarcomas and all Kaposi's sarcomas showed mixed expression of both lymphatic and blood vascular endothelial phenotypes. By double lab

关键词：抗原 CD31/代谢抗原 CD34/代谢毛细血管/代谢毛细血管/病理学细胞培养的内皮淋巴管/代谢内皮淋巴管/病理学内皮血管/代谢内皮血管/病理学因子Ⅷ/代谢荧光抗体技术间接血管肉瘤/血液供给血管肉瘤/代谢血管肉瘤/病理学免疫酶技术膜糖蛋白类/免疫学膜糖蛋白类/代谢受体蛋白质酪氨酸激酶类/代谢受体细胞表面/代谢唾液糖蛋白类/代谢肿瘤标记生物学/分析血管内皮生长因子受体3 血管肿瘤/血液供给血管肿瘤/代谢血管肿瘤/病理学人类

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GENOMICS 2000年第1期66卷 98-103页

作者： Baust, C Seifarth, W Germaier, H Hehlmann, R Leib-Mösch, C Univ Heidelberg Fac Clin Med Mannheim Med Clin 3 D-68305 Mannheim Germany Inst Mol Virol Res Ctr Environm & Hlth D-85758 Oberschleissheim Germany

The human genome harbors thousands of long terminal repeats (LTRs) that are derived from endogenous retroviruses and contain elements able to regulate the expression of neighboring cellular genes. We have investigated the ability of human endogenous retroviral (HERV)-K LTRs to provide transcriptional processing signals for nonviral sequences. Four chimeric cDNA clones isolated from a cDNA library derived from the human cell line T47D were found to be polyadenylated within an HERV-K-T47D-related LTR. Two transcripts containing an as yet unknown cellular sequence were probably derived from the same genomic locus but their 3' ends were processed at different positions of the LTR. Structural analysis of the, polyadenylation site suggests RNA stem-loop structures similar to the HTLV-1 Rex responsive element that bring the two remote AAUAAA and GU-rich elements into the spatial juxtaposition necessary for correct 3' end processing. The cellular part of the third chimeric clone shows significant homology to an exon of the human tyrosine phosphatase 1 gene, although oriented in the antisense direction compared to the adjacent LTR. Furthermore, we found that the 3' untranslated region of the human transmembrane tyrosine kinase gene FLT4 is probably derived from a partial HERV-K-T47D LTR sequence. Taken together, our data suggest that LTRs of the HERV-K-T47D family display biological function by mediating polyadenylation of cellular sequences. (C) 2000 Academic Press.

关键词： 3'非翻译区碱基序列嵌合体克隆分子 DNA探针内源性逆转录病毒/遗传学基因表达调控基因文库基因组人分子序列数据核酸构象聚腺苷酸类/代谢 RNA 信使/代谢受体蛋白质酪氨酸激酶类/遗传学受体细胞表面/遗传学序列同源性核酸末端重复序列/遗传学转录遗传/遗传学肿瘤细胞培养的血管内皮生长因子受体3 人类

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VEGF-C、VEGF-D及其受体FLt-4与大肠癌淋巴转移及预后的相关性研究

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河北医学 2007年第10期13卷 1135-1140页

作者：杨诚孙少杰薛伟山宋修岐青岛大学医学院第二附属医院普外科山东青岛266042

目的:研究VEGF-C、VEGF-D及其受体Flt-4在大肠癌组织中的表达规律,探讨其与大肠癌浸润特点、淋巴转移等生物学特性及预后的关系。方法:采用免疫组织化学染色法检测45例大肠癌组织中VEGF-C、VEGF-D及Flt-4表达情况,评估VEGF-C、VEGF-D及F... 详细信息

目的:研究VEGF-C、VEGF-D及其受体Flt-4在大肠癌组织中的表达规律,探讨其与大肠癌浸润特点、淋巴转移等生物学特性及预后的关系。方法:采用免疫组织化学染色法检测45例大肠癌组织中VEGF-C、VEGF-D及Flt-4表达情况,评估VEGF-C、VEGF-D及Flt-4的表达与大肠癌生物学特性及预后的关系。结果:研究发现大肠癌组织VEGF-C和VEGF-D及其受体Flt-4阳性表达率显著高于正常组织(P<0.05)。并且VEGF-C/VEGF-D表达与Flt-4蛋白表达呈显著正相关(P<0.01)。VEGF-C、VEGF-D及Flt-4的表达在有无淋巴管浸润组、有无淋巴结转移组及不同Dukes分期中亦有显著性差异(P<0.05),45例大肠癌患者术后5年生存率为53.3%。其中VEGF-C、VEGF-D和Flt-4阳性患者5年生存率均分别低于阴性患者组(P<0.05)。结论:在大肠癌组织中VEGF-C和VEGF-D与其受体Flt-4的表达与大肠癌淋巴管的发生及促进肿瘤细胞经淋巴管转移可能起一定作用,VEGF-C和VEGF-D表达的检测可作为预测大肠癌淋巴结转移的辅助指标;VEGF-C和VEGF-D蛋白高表达与大肠癌患者预后相关,可能成为今后大肠癌预后评估的分子指标之一。

关键词：血管内皮生长因子C 血管内皮生长因子D 血管内皮生长因子受体3 大肠肿瘤:免疫组化

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金雀异黄素对肺癌细胞生长、侵袭和转移的影响

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江苏医药 2018年第12期44卷 1361-1365,F0002,F0003页

作者：邢晓莉曾妮刘振宽白玉霞王艳黄少祥天津市第五中心医院呼吸科 300450

目的探讨金雀异黄素对人肺癌细胞生长、侵袭和转移的影响及其机制。方法金雀异黄素处理体外培养的人肺癌A549和H358细胞,采用MTT法检测细胞活力,集落形成实验观察细胞生长,流式细胞术分析细胞凋亡,细胞迁移与侵袭实验观察对肺癌细胞迁... 详细信息

目的探讨金雀异黄素对人肺癌细胞生长、侵袭和转移的影响及其机制。方法金雀异黄素处理体外培养的人肺癌A549和H358细胞,采用MTT法检测细胞活力,集落形成实验观察细胞生长,流式细胞术分析细胞凋亡,细胞迁移与侵袭实验观察对肺癌细胞迁移和侵袭的影响。在裸鼠体内注入绿荧光素酶标记的肺癌A549细胞,观察金雀异黄素对肺癌细胞体内生长和转移的影响。采用qRT-PCR和Western blot分析金雀异黄素对肺癌细胞转移相关mRNA和蛋白表达的影响。结果金雀异黄素可以抑制肺癌A549和H358细胞的生长。金雀异黄素能引起肺癌细胞凋亡增加(P<0.01)。金雀异黄素可以抑制体外和体内肺癌细胞的迁移和侵袭(P<0.01)。金雀异黄素能下调MMP-9和血管内皮生长因子受体3(VEGFR3)mRNA和蛋白的表达。结论金雀异黄素能抑制肺癌细胞生长、侵袭和转移;其机制可能与下调MMP-9和VEGFR3的表达有关。

关键词：肺癌金雀异黄素基质金属蛋白酶9 血管内皮生长因子受体3

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