神经型钙黏蛋白分子在多发性骨髓瘤患者中的表达

目的 探讨神经型钙黏蛋白（N-cadherin）分子在多发性骨髓瘤（MM）患者中的表达及其临床意义.方法 收集54例初治MM患者及20名健康人骨髓单个核细胞,应用实时荧光定量PCR法检测N-cadherin mRNA表达,Western blot法测定其蛋白表达.结果 MM患者N-cadherin mRNA表达水平为6.056±3.033,健康对照组为1.788±0.778,二组相比差异有统计学意义（P＜0.0001）.按照ISS分期,Ⅰ期、Ⅱ期、Ⅲ期MM患者N-cadherin mRNA表达水平分别为3.681±3.185、5.757±3.292、7.460±3.647,其中Ⅱ期、Ⅲ期与健康对照组相比差异均具有统计学意义（均P＜0.05）;Ⅰ期与健康对照组相比差异无统计学意义（P＞0.05）.有髓外浸润及无髓外浸润患者N-cadherin mRNA表达量分别为9.159±3.178、5.083±3.288,差异有统计学意义（P＜ 0.001）.有骨质破坏和无骨质破坏患者N-cadherin mRNA表达量分别为6.544±3.729、4.240±2.896,差异有统计学意义（P=0.047）.初治MM患者N-cadherin mRNA表达水平为6.056±3.033,治疗后有效患者N-cadherin mRNA表达水平下降（3.768±2.216）（P=0.015）,治疗无效患者N-cadherin mRNA水平与治疗前相比差异无统计学意义（P＞0.05）.初治MM患者N-cadherin蛋白表达量明显高于缓解期患者及健康对照组,而在治疗后复发的患者中,N-cadherin蛋白表达量明显高于初治患者.结论 N-cadherin分子在MM患者中高表达,其可能参与MM的发生及发展.     

白藜芦醇对卵巢癌细胞增殖活力、增殖基因mRNA表达及Wnt信号通路的影响

目的研究白藜芦醇对卵巢癌细胞增殖活力、增殖基因mRNA表达及Wnt信号通路的影响。方法培养卵巢癌SKOV3细胞株,并随机分为四组,对照组用不含药物的DMEM处理,白藜芦醇组用含有不同剂量(20、40、80μmol/L)的白藜芦醇处理。处理24 h后,使用酶标仪检测表示细胞增殖活力的光密度(OD_(490))值,荧光定量PCR检测细胞周期基因c-myc、细胞周期蛋白A(cyclin A)、细胞周期蛋白D1(cyclin D1)、p21及上皮间质转化基因N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、E-钙黏蛋白(E-cadherin)的mRNA表达水平,Western blotting法检测Wnt信号通路分子糖原合成激酶-3β(GSK-3β)和β-连环蛋白(β-catenin)的蛋白表达水平。结果 20、40、80μmol/L白藜芦醇组SKOV3细胞的OD_(490)值、细胞中c-myc、cyclin A、cyclin D1、N-cadherin、Vimentin的mRNA表达水平及β-catenin的蛋白表达水平均明显低于对照组,细胞中p21、E-cadherin的mRNA表达水平及GSK-3β的蛋白表达水平均明显高于对照组,且随着白藜芦醇剂量的升高,SKOV3细胞的OD_(490)值、细胞中c-myc、cyclin A、cyclin D1、N-cadherin、Vimentin的mRNA表达水平及β-catenin的蛋白表达水平逐渐下降,细胞中p21、E-cadherin的mRNA表达水平及GSK-3β的蛋白表达水平逐渐升高,差异均有统计学意义(P0.05)。结论白藜芦醇能够以剂量依赖性的方式降低卵巢癌细胞的增殖活力、调节增殖基因的表达,且这一作用与Wnt信号通路激活的受抑制有关。     

5-氮杂-2＇-脱氧胞苷对人卵巢癌细胞株RASSF1A基因表达的影响

目的 观察5-氮杂-2＇-脱氧胞苷（5-Aza-CdR）对体外培养的人卵巢癌细胞株（SKOV3、3AO） RASSF1A mRNA及蛋白表达的影响.方法 卵巢癌细胞株（SKOV3、3AO）经不同浓度（0.5、5、50 μmol/L）的5-Aza-CdR处理,未经处理的作为对照组,反转录聚合酶链反应（RT-PCR）及免疫印记（Western Blot）检测RASSF1A在mRNA和蛋白质水平表达的变化.结果 对照组细胞株SKOV3、3AO均可见RASSF1A mRNA及蛋白的表达,但表达较弱,经药物处理后的细胞RASSF1A mRNA及蛋白的表达较前明显增强.经不同浓度5-Aza-cdR处理的SKOV3细胞株中,随浓度增加,RASSF1A mRNA及蛋白的表达依次递增.经不同浓度5-Aza-cdR处理的3AO细胞株中,经0.5μmol/L 5-Aza-cdR处理后,RASSF1A mRNA的表达明显低于经5和50 μmol/L 5-Aza-cdR处理后的表达（t=-8.866,P=0.01;t=-12.256,P=0.000）;但经5、50 μmol/L 5-Aza-cdR分别处理的3AO细胞株RASSF1A mRNA的表达差异无统计学意义（t=0.431,P=0.689）.在3AO细胞株中,0.5 μmol/L组与5μmol/L组RASSF1A蛋白表达差异无统计学意义（t=-1.586,P=0.188）.结论 经过5-Aza-CdR处理后,卵巢癌细胞株（SKOV3、3AO） RASSF1A mRNA及蛋白的表达均明显增强,细胞增殖能力受到明显抑制,从而起到抑制肿瘤细胞生长,甚至促进肿瘤细胞凋亡的作用.     

芬太尼调控LINC00184抑制卵巢癌SKOV3细胞增殖和侵袭

目的:研究芬太尼对卵巢癌SKOV3细胞增殖、凋亡和侵袭等生物学行为的影响,并探讨其作用机制。方法:体外培养人卵巢癌SKOV3细胞,采用CCK-8实验、克隆形成实验检测芬太尼对SKOV3细胞体外增殖的影响;分别采用流式细胞术和Transwell实验检测芬太尼对SKOV3细胞凋亡和侵袭能力的影响;Western blot检测细胞增殖、凋亡及侵袭相关蛋白表达。qRT-PCR检测LINC00184在卵巢癌细胞系和正常卵巢上皮细胞株的表达;构建LINC00184过表达质粒并转染SKOV3细胞,观察上调LINC00184表达对芬太尼处理的SKOV3细胞增殖、凋亡及侵袭的影响。结果:芬太尼在体外呈时间和浓度依赖性抑制SKOV3细胞存活,而不明显影响正常卵巢上皮细胞HOSE的存活率。相比对照组,使用5 ng/mL和10 ng/mL芬太尼处理SKOV3细胞,显著下调LINC00184表达水平,降低体外克隆形成率,抑制Ki67、PCNA蛋白表达（均P＜0.01）;显著增加SKOV3细胞凋亡率,上调Bax蛋白表达,下调Bcl-2蛋白表达（均P＜0.01）;显著降低侵袭细胞数,上调E-cadherin蛋白表达,下调N-cadherin、MMP9蛋白表达（均P＜0.01）。而使用LINC00184过表达质粒上调LINC00184表达则明显削弱芬太尼对SKOV3细胞的上述作用（P＜0.01）。结论:LINC00184在卵巢癌细胞表达上调,并与卵巢癌细胞的增殖、凋亡和侵袭等生物学特性相关;芬太尼通过下调LINC00184表达抑制卵巢癌细胞的增殖和侵袭,并诱导其凋亡。     

5-氮-2''-脱氧胞苷对人卵巢癌细胞凋亡及DNA错配修复基因表达的影响

目的:观察5-氮-2'-脱氧胞苷(5-aza-2'-deoxycytidine ,又称5-aza-CdR)对卵巢癌细胞SKOV3和3AO增殖凋亡及DNA错配基因hMLH1 和hMLH2 表达的影响.方法: 以特异性甲基转移酶抑制剂5-aza-CdR 0.5、5、50μmol/L处理人卵巢癌细胞SKOV3和3AO 3d,继续常规培养7 d后,采用MTT比色法观察细胞经药物处理前后的增殖活性,用流式细胞术分析5-aza-CdR对细胞凋亡影响,以半定量逆转录-聚合酶链反应(RT-PCR)检测细胞经5-aza-CdR处理前后DNA错配修复基因hMLH1和hMSH2 mRNA表达水平的改变.结果: 人卵巢癌细胞SKOV3和3AO经5-aza-CdR处理后,与对照组比较,0.5、5、50 μmol/L均能明显抑制肿瘤细胞生长,随着5-aza-CdR浓度增加,细胞增殖速度下降.SKOV3经5-aza-CdR 0.5、5、50μmol/L处理后细胞的凋亡率分别为(10.59±1.57)%、(17.52±1.72)%、(34.10±1.45)%,3A0经0.5、5、50μmol/L 5-aza-CdR处理后细胞的凋亡率分别为(11.11±2.21)%、(17.24±1.11)%、(26.53±2.00)%,与对照组相比均有统计学意义(P＜0.01);且凋亡率与剂量成正相关(FSKOV3=227.6,P SKOV3＜0.01;F3AO=108.4,P 3AO＜0.01).经5-aza-CdR处理后的两株卵巢癌细胞中hMLH1 和hMLH2 的mRNA表达量有不同程度的增加(P＜0.01),且与药物存在剂量依赖性.结论: 在人卵巢癌细胞株SKOV3和3AO中,5-aza-CdR可部分逆转hMLH1 和hMLH2 的失活,恢复其生长调控功能,抑制肿瘤细胞生长,并诱导细胞凋亡.     

熊果酸联合顺铂对卵巢癌干细胞的增殖、凋亡、侵袭和迁移的影响

目的:观察熊果酸（ursolic acid,UA）联合顺铂(DDP)对卵巢癌干细胞增殖、凋亡、侵袭及迁移能力的影响及其作用机制。方法:通过体外无血清悬浮培养人卵巢癌SKOV3干细胞并进行细胞鉴定。实验分为SKOV3干细胞组、熊果酸组、熊果酸联合顺铂组。MTT法检测干细胞的增殖,Transwell实验检测干细胞侵袭与迁移能力,采用Annexin V/PI双染法流式细胞术检测干细胞凋亡。Real-time PCR检测上皮间质转化（epithelial-mesenchymal transition,EMT）相关标记分子Vimentin、N-cadherin、E-cadherin、Fibronectin、Twist的mRNA表达情况,Western-blot检测E-cadherin、Vimentin、Twist蛋白表达情况。结果:熊果酸对SKOV3干细胞增殖有显著抑制作用,呈剂量依赖性（P＜0.05）;流式细胞术显示熊果酸组、熊果酸联合顺铂组均可提高SKOV3干细胞的凋亡率,与SKOV3干细胞组相比有统计学差异（P＜0.05）;熊果酸组、熊果酸联合顺铂组可有效抑制SKOV3干细胞的侵袭和迁移能力（P＜0.05）;Real-time PCR测定熊果酸组、熊果酸联合顺铂组作用SKOV3干细胞后EMT基因表达水平,结果显示Fibronectin、Twist、Vimentin、N-cadherin表达降低,E-cadherin表达升高（P＜0.05）;Western-blot结果显示熊果酸组、熊果酸联合顺铂组可上调E-cadherin蛋白的表达,下调Vimentin、Twist蛋白的表达;与熊果酸组相比,熊果酸联合顺铂组对干细胞凋亡率更高,迁移和侵袭能力更低,E-cadherin表达更高,Vimentin和Twist表达更低,以上差异均有统计学意义（P＜0.05）。结论:熊果酸对卵巢癌干细胞有抑制增殖、侵袭和迁移,诱导凋亡的作用,联合顺铂作用效果更优,其机制可能与逆转EMT有关。     

STAT 3通过ZEB1调节卵巢癌细胞SKOV-3中E-cadherin表达的研究

目的:探讨卵巢癌细胞SKOV-3中信号转导与转录激活因子3(STAT3)对上皮细胞钙黏蛋白(Ecadherin)表达的调控.方法:构建STAT 3过表达载体或缺失表达载体,并转染SKOV-3细胞,分别用Western blotting和RT-PCR方法检测STAT 3 mRNA及蛋白质水平的变化,确定细胞模型的建立.Western blotting检测构建的细胞模型中p-STAT 3水平与E-cadherin水平的变化,RT-PCR检测STAT 3过表达或缺失对ZEB1和ZEB2 mRNA水平的影响.同时构建ZEB1 siRNA与pCDNA3.1-STAT 3共转染细胞,Westernblotting检测ZEB1对p-STAT 3诱导的E-cadherin水平下调的影响.结果:STAT 3过表达/缺失载体的SKOV-3细胞中E-cadherin蛋白质水平显著下调/上调;STAT 3过表达能显著上调ZEB1 mRNA水平,但对ZEB2 mRNA无显著影响;ZEB1 siRNA转染能逆转STAT 3过表达诱导的E-cadherin的水平下降.结论:卵巢癌细胞SKOV-3中,STAT 3能通过ZEB1调节E-cadherin的表达,在卵巢癌的发生发展中起重要作用.     

干扰Plexin-B1对卵巢癌SKOV3细胞自噬和顺铂敏感性的影响

目的:探讨干扰丛状蛋白B1(Plexin-B1)对卵巢癌SKOV3细胞自噬和顺铂敏感性的影响。方法:合成Plexin-B1的siRNA序列和NC序列,转染至卵巢癌SKOV3细胞,qRT-PCR检测转染效率。将细胞分为对照组、NC组和si-Plexin-B1组,CCK8检测细胞活性,qRT-PCR法检测细胞中Plexin-B1 mRNA的表达,Western blot法检测细胞中Plexin-B1、Akt、p-Akt、LC3-Ⅱ、CALR和PRKDC蛋白的表达。不同浓度的顺铂(1、2、4、8、16、32μg/mL)处理细胞,CCK8检测各组细胞增殖情况,评估干扰Plexin-B1对顺铂敏感性的影响。结果:与对照组相比,干扰Plexin-B1后卵巢癌SKOV3细胞活性、细胞中Plexin-B1 mRNA和蛋白表达水平及Akt蛋白的磷酸化水平均显著降低(P<0.05),细胞中LC3-Ⅱ、CALR和PRKDC蛋白表达水平均显著升高(P<0.05)。CCK8检测结果显示,卵巢癌SKOV3细胞增殖能力随着顺铂浓度的升高逐渐降低,且干扰Plexin-B1后卵巢癌SKOV3细胞的增殖能力较...     

5-氮-2′-脱氧胞苷对人卵巢癌细胞凋亡及DNA错配修复基因表达的影响

目的:观察5-氮-2′-脱氧胞苷(5-aza-2′-deoxycytidine,又称5-aza-CdR)对卵巢癌细胞SKOV3和3AO增殖凋亡及DNA错配基因hMLH1和hMLH2表达的影响。方法:以特异性甲基转移酶抑制剂5-aza-CdR0.5、5、50μmol/L处理人卵巢癌细胞SKOV3和3AO3d,继续常规培养7d后,采用MTT比色法观察细胞经药物处理前后的增殖活性,用流式细胞术分析5-aza-CdR对细胞凋亡影响,以半定量逆转录-聚合酶链反应(RT-PCR)检测细胞经5-aza-CdR处理前后DNA错配修复基因hMLH1和hMSH2mRNA表达水平的改变。结果:人卵巢癌细胞SKOV3和3AO经5-aza-CdR处理后,与对照组比较,0.5、5、50μmol/L均能明显抑制肿瘤细胞生长,随着5-aza-CdR浓度增加,细胞增殖速度下降。SKOV3经5-aza-CdR0.5、5、50μmol/L处理后细胞的凋亡率分别为(10.59±1.57)%、(17.52±1.72)%、(34.10±1.45)%,3A0经0.5、5、50μmol/L5-aza-CdR处理后细胞的凋亡率分别为(11.11±2.21)%、(17.24±1.11)%、(26.53±2.00)%,与对照组相比均有统计学意义(P<0.01);且凋亡率与剂量成正相关(FSKOV3=227.6,PSKOV3<0.01;F3AO=108.4,P3AO<0.01)。经5-aza-CdR处理后的两株卵巢癌细胞中hMLH1和hMLH2的mRNA表达量有不同程度的增加(P<0.01),且与药物存在剂量依赖性。结论:在人卵巢癌细胞株SKOV3和3AO中,5-aza-CdR可部分逆转hMLH1和hMLH2的失活,恢复其生长调控功能,抑制肿瘤细胞生长,并诱导细胞凋亡。     

HPV16E6 siRNA联合5-Aza-CdR对宫颈癌SiHa细胞中E-钙黏蛋白表达和基因甲基化的影响

目的:探讨HPV16E6 siRNA联合5-Aza-CdR(5-aza-2'-deoxycytidine,5-氮-2'-脱氧胞苷,又称地西他滨)对宫颈癌SiHa细胞中E-钙黏蛋白表达和基因甲基化的影响。方法:采用SiHa细胞构建的HPV16E6 沉默细胞株及5-Aza-CdR细胞株,检测细胞中E-cadherin mRNA和蛋白表达,以及E-cadherin甲基化状态。采用细胞黏附、Transwell体外侵袭、迁移实验检测5-Aza-CdR和siRNA E6对SiHa细胞黏附、侵袭迁移的影响。结果:5-Aza-CdR+siRNA E6组较5-Aza-CdR组、siRNA E6组中E-cadherin mRNA 及蛋白表达均上升,细胞的黏附率、侵袭抑制率和迁移抑制率均升高;5-Aza-CdR+siRNA E6组较5-Aza-CdR组、siRNA E6组中E-cadherin基因启动子区甲基化指数明显下降。结论:HPV16E6 siRNA联合5-Aza-CdR可显著引起宫颈癌细胞中E-cadherin 基因低甲基化,并可导致E-cadherin mRNA 及蛋白的表达水平明显上调,肿瘤细胞黏附能力升高,侵袭迁移能力下降,两者在一定程度起到协同作用。     

E-钙粘蛋白与肿瘤转移

钙粘蛋白是一组跨膜糖蛋白,主要参与同源细胞之间的连接,分为E、P和N三种。其中,E-钙粘蛋白主要分布在各种上皮细胞,E-钙粘蛋白具有抑制转移的作用,肿瘤细胞中E-钙粘蛋白基因的丢失,可导致细胞的侵袭和转移潜能的增加。本文就E-钙粘蛋白与肿瘤转移做简单综述。     

Beyond a tumor suppressor: Soluble E‐cadherin promotes the progression of cancer

E‐cadherin (E‐cad) plays important roles in tumorigenesis as well as in tumor progression, invasion and metastasis. This protein exists in two forms: a membrane‐tethered form and a soluble form. Full‐length E‐cad is membrane tethered. As a type I transmembrane glycoprotein, E‐cad mainly mediates adherens junctions between cells and is involved in maintaining the normal structure of epithelial tissues. Soluble E‐cad (sE‐cad) is the extracellular fragment of the protein that is cleaved from the membrane after proteolysis of full‐length E‐cad. The production of sE‐cad undermines adherens junctions, causing a reduction in cell aggregation capacity; furthermore, sE‐cad can diffuse into the extracellular environment and the blood. As a paracrine/autocrine signaling molecule, sE‐cad activates or inhibits multiple signaling pathways and participates in the progression of various types of cancer, such as breast cancer, ovarian cancer, and lung cancer, by promoting invasion and metastasis. This article briefly reviews the role of sE‐cad in tumorigenesis and tumor progression and its significance in clinical therapeutics.     

CDH1 and CDH13 methylation in serum is an independent prognostic marker in cervical cancer patients

Cervical cancer is the principal cause of death due to cancer in women. Five-year survival rate ranges from 15-80%, depending on the extent of the disease. New predictive markers for relapse may increase survival rates by improving treatment of patients at high risk for relapse. The gene products of CDH1 and CDH13, namely E-cadherin and H-cadherin, play a key role in cell-cell adhesion. Inactivation of the cadherin-mediated cell adhesion system, caused by aberrant methylation, is a common finding in human cancers. To test the hypothesis that CDH1/CDH13 methylation is a prognostic marker in cervical cancer we determined the methylation status of CDH1/CDH13 in serum samples from 93 cervical cancer patients. Methylation analysis was carried out using MethyLight. Aberrant methylation of the 5'-region of CDH1 or CDH13 was observed in 43% (40 of 93) of the patients. Cervical cancer patients with unmethylated CDH1/CDH13 in serum samples showed significantly better disease-free survival in univariate and multivariate analysis. Median disease-free survival for CDH1/CDH13 methylation negative and positive patients was 4.3 years and 1.2 years, respectively. Our results suggest that detection of aberrant methylation of CDH1/CDH13 may be of potential use as a marker for selecting cervical cancer patients at high risk for relapse who could benefit from additional systemic therapy.     

ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression

Pancreatic cancer is one of the most aggressive malignant diseases. We recently reported that N-cadherin plays a key role in tumor progression and metastasis in pancreatic cancer. For this study, we sought to determine if an N-cadherin-blocking peptide (ADH-1) could prevent N-cadherin-mediated tumor progression in a mouse model for pancreatic cancer. The effect of ADH-1 on N-cadherin-mediated cell scattering and migration on collagen I was examined using pancreatic cancer cells. We also examined the influence of ADH-1 on cell apoptosis. Furthermore, in vivo animal studies were performed using orthotopic injection of N-cadherin overexpressing BxPC-3 cells with or without ADH-1 treatment. BxPC-3 and Capan-1 cells exhibited increased expression of N-cadherin in response to collagen I. This increase in N-cadherin promoted cell scattering and migration in response to collagen I. ADH-1 prevented these changes, but did not inhibit upregulation of N-cadherin. TUNEL assays and immunoblots for caspase-3 showed that ADH-1 induced apoptosis in a concentration dependent and N-cadherin dependent manner in pancreatic cancer cells. ADH-1 treatment resulted in significant reductions in tumor growth and lung metastasis in a mouse model for pancreatic cancer. The N-cadherin antagonist, ADH-1 has significant antitumor activity against N-cadherin-expressing cells using in vitro assays and in an orthotopic mouse model for pancreatic cancer, raising the possibility that N-cadherin antagonists have therapeutic potential for the treatment of pancreatic cancer in humans.     

Prognostic value of E-cadherin immunoexpression in patients with primary ovarian carcinomas.

PURPOSE: To analyse the negative versus positive immunoexpression of E-cadherin in patients with primary ovarian carcinomas, and determine its significance in relation to clinicopathological features, overall and recurrence-free survival (RFS). PATIENTS AND METHODS: The protein expression of E-cadherin was immunohistochemically evaluated in formalin-fixed, paraffin-embedded samples in 104 patients with primary ovarian carcinomas. The clinicopathological factors studied were age, FIGO staging, histological type, tumour differentiation, the appearance of the ovarian capsule, peritoneal implants and residual tumour after cytoreductive surgery. Overall survival and RFS were evaluated using the Kaplan-Meier method, and multivariate analysis was completed using the Cox regression model. RESULTS: Of the 104 carcinomas, negative E-cadherin immunoexpression was observed in seven (7%) cases, and positive immunoexpression in 97 (93%). E-cadherin categorised into negative versus positive expression did not associate with any of the established clinicopathological parameters. However, negative E-cadherin expression significantly predicted a poorer overall survival when compared with positive expression (P=0.006). In the multivariate analyses, negative E-cadherin and the presence of residual tumour after cytoreductive surgery were independent prognostic factors for survival (P=0.014 and P=0.034, respectively). CONCLUSIONS: The presence of residual tumour after primary cytoreductive surgery and negative E-cadherin expression seem to be useful markers in patients with ovarian carcinomas likely to have an unfavourable clinical outcome. The assessment of E-cadherin immunoreactivity may be a useful prognostic indicator in ovarian cancer, complementary to established prognostic factors.     

Desmocollin switching in colorectal cancer

The desmocollins are members of the desmosomal cadherin family of cell-cell adhesion molecules. They are essential constituents of desmosomes, intercellular junctions that play a critical role in the maintenance of tissue integrity in epithelia and cardiac muscle. In humans, three desmocollins (Dsc1, Dsc2 and Dsc3) have been described. The desmocollins exhibit tissue-specific patterns of expression; only Dsc2 is expressed in normal colonic epithelium. We have found switching between desmocollins in sporadic colorectal adenocarcinoma with a reduction in Dsc2 protein (in 8/16 samples analysed by immunohistochemistry) being accompanied by de novo expression of Dsc1 (16/16) and Dsc3 (7/16). Similar results were obtained by western blotting of a further 16 samples. No change was found in Dsc2 mRNA, but de novo expression of Dscs 1 and 3 was accompanied by increased message levels. Loss of Dsc2 (8/19) and de novo expression of Dsc1 (11/19) and Dsc3 (6/19) was also found in colorectal adenocarcinomas on a background of colitis. The data raise the possibility that switching of desmocollins could play an important role in the development of colorectal cancer.     

缺氧对乳腺癌 MCF -7 细胞中 LOXL2 及 E - 钙粘蛋白表达的影响

目的：观察缺氧对乳腺癌MCF-7细胞中LOXL2和E-钙粘蛋白表达的影响。方法：使用Westernblot、real—timePCR分别在蛋白和mRNA水平观察缺氧如何调节乳腺癌MCF-7细胞中LOXL2和E一钙粘蛋白的表达。结果：在乳腺癌MCF-7细胞中,缺氧上调LOXL2蛋白和mRNA表达,下调E-钙粘蛋白和mRNA水平。结论：缺氧调节乳腺癌细胞中LOXL2及E-钙粘蛋白基因的表达,为进一步探讨乳腺癌发病机制及治疗提供有力证据。     

结直肠癌组织中E-钙黏素表达及其临床意义

目的　探讨E -钙黏素在结直肠癌组织中的变化及其与结直肠癌临床病理因素的关系。方法　应用免疫组化方法检测 5 2例结直肠癌、10例结直肠腺瘤、8例正常肠黏膜组织中E -钙黏素的表达情况。结果　结直肠癌E -钙黏素弱表达率或阴性表达率 (3 4.6% ,3 6.6% )明显高于结直肠腺瘤、正常肠组织 (P <0 .0 5 ) ;E -钙黏素表达与结直肠癌远处转移明显相关 (P <0 .0 5 ) ,与肿瘤大小、淋巴结侵犯、浆膜浸润无关 (P >0 .0 5 ) ,低分化者E -钙黏素弱表达率或阴性表达率明显高于中分化、高分化者(P <0 .0 5 ) ,随Duke分期进展 ,E -钙黏素阴性表达率或弱表达率逐渐增高 ,DukeD、C与DukeB、A比较有显著性差异 (P <0 .0 5 )。结论　E -钙黏素与结直肠癌生物学行为密切相关。     

E-钙粘附素的表达与胃癌临床病理特征的关系

目的：探讨 Ｅ钙粘附素（ Ｅ Ｃ Ｄ） 表达与胃癌生物学行为的关系。方法：采用免疫组化染色方法检测８０ 例胃癌组织 Ｅ Ｃ Ｄ 的表达情况。结果：正常胃粘膜呈 Ｅ Ｃ Ｄ 保留表达，８６３ ％ （６９／８０） 的胃癌 Ｅ Ｃ Ｄ 表达减弱或消失； Ｅ Ｃ Ｄ 表达减弱与胃癌浸润型生长及分化较差密切相关（ Ｐ＜ ００１） ，而与胃癌浸润深度、淋巴结转移、静脉、淋巴管润浸无关（ Ｐ＞ ００５） 。结论： Ｅ Ｃ Ｄ 的表达可能决定着胃癌的生长方式和分化程度，而与胃癌侵袭转移潜能无关。