γ-谷胱甘肽环酰基转移酶在结直肠癌中的表达及临床意义

目的检测γ-谷胱甘肽环酰基转移酶(γ-glutamyl cyclotransferase,GGCT)在结直肠癌(colorectal cancer, CRC组织中的表达,探讨GGCT表达与患者临床病理特征、结直肠肿瘤细胞增殖的关系,进一步探究GGCT表达与CRC患者预后的相关性。方法采用免疫组织化学方法检测229例结直肠肿瘤组织和其中能收集到的167例癌旁正常组织中GGCT、Ki-67和细胞周期蛋白D1 (cyclin D1)的表达水平,应用SPSS 26.0软件对实验数据进行统计学处理。结果 GGCT在CRC和癌旁组织的胞质阳性表达率分别为83.4%和75.4%(P=0.792),而在胞核的阳性表达率分别为36.7%和74.3%(P=0.045);Ki-67在CRC和癌旁正常组织阳性表达率分别为77.7%和60.5%(P=0.040);cyclin D1在CRC和癌旁正常组织阳性表达率分别为43.2%和12.0%(P=0.030)。GGCT在细胞核中阳性表达与肿瘤大小、淋巴结转移、TNM分期呈负相关,GGCT在CRC组织中的表达与Ki-67、cyclin D1呈负相关。CRC患者中GGCT核阴性表达组生存期低于阳性表达组。结论 GGCT在CRC和癌旁正常组织细胞中的定位存在差异,这一差异主要体现在细胞核上。GGCT在CRC胞核中低表达,癌旁正常组织中高表达。GGCT在CRC细胞中的定位不同,发挥功能不同,胞核上GGCT表达的降低可能与肿瘤细胞增殖活性增加有关,与CRC患者生存预后有关,参与了CRC的发生与发展。     

CD133和maspin在肝癌中的表达及其临床病理意义

目的 探讨肿瘤干细胞标志物CD133和maspin在肝细胞性肝癌（hepatocellular carcinoma HCC）中的表达情况及其临床病理意义.方法 采用免疫组织化学ElivisionTM plus法检测100例HCC组织和20例癌旁肝组织中CD133和maspin蛋白的表达情况.结果 在癌旁肝组织中CD133和maspin蛋白的阳性表达率分别为5.0%和100%,而在HCC组中其阳性表达率分别为51.0%和48.0%,两组之间差异有显著性（P〈0.01）.CD133蛋白的表达水平与肿瘤的Edmondson分级、淋巴结转移、肿瘤的数目和有无血管侵犯有关（全部P〈0.05）;maspin蛋白的表达水平与肿瘤的Edmondson分级、肿瘤的数目和有无血管侵犯有关（全部P〈0.05）.且CD133蛋白的表达与maspin蛋白的表达呈负相关（P〈0.01）.结论 CD133和maspin蛋白的表达与HCC组织的Edmondson分级、肿瘤数目和血管侵犯有关;CD133和maspin的联合检测对HCC的进展及预后判断有重要意义.     

细胞周期蛋白B1、D1和E真核表达载体的构建及表达

目的：为研究细胞周期蛋白（cyclin）在肿瘤形成过程中的分子机制,构建带FLAG标签的细胞周期蛋白B1、D1、E的真核表达载体,并检测其在293T细胞中的表达。方法：以乳腺cDNA文库为模板,分别扩增细胞周期蛋白B1、D1、E基因全长编码区序列,克隆到pcDNA3-FLAG真核表达载体上;用脂质体介导的基因瞬时转染法,将重组正确的表达载体转染293T细胞,检测细胞中的FLAG融合蛋白的表达。结果：酶切鉴定和DNA序列分析显示构建了正确的FLAG-Cyclin真核表达载体,Western印迹分析表明克隆的载体都能在真核细胞中表达分子大小相符的重组蛋白。结论：构建了FLAG-CyclinBl、FIAG-CyclinDl、FLAG-CyclinE真核表达载体,为细胞周期蛋白及其相关蛋白的研究奠定了基础。     

反义细胞周期蛋白E真核表达载体的构建及其对体外人乳腺癌细胞的抑制作用

 为了探讨细胞周期蛋白 E(cyclin E)与人乳腺癌细胞恶性特征间的相关性 ,利用反义 RNA抑制基因表达的技术 ,构建了细胞周期蛋白 E反义 RNA的真核表达载体并转入人乳腺癌细胞中 .通过 G41 8筛选出阳性克隆 ,经 PCR和 Western印迹检测 ,确定细胞中含有重组质粒 ,并且细胞周期蛋白 E蛋白的水平明显降低 ,由此获得了反义 RNA表达载体导致的细胞周期蛋白 E表达受抑制的细胞 .细胞模型建立后 ,观察分析了细胞形态 ,细胞生长的血清依赖性以及软琼脂成集落能力 ,与对照细胞相比所发生的变化 .结果显示 ,细胞周期蛋白 E受抑制后 ,乳腺癌细胞体积变大 ,细胞生长对血清依赖性增加 ,低血清培养到第 6d时 ,细胞密度约为对照细胞的五分之一 ,细胞成集落能力也显著下降 ,软琼脂中克隆形成率下降 57% .这些变化都表明乳腺癌细胞恶性程度由于细胞周期蛋白 E表达受抑制而减弱 ,可以推测 cyclin E与乳腺癌细胞的恶性增殖及非锚定依赖性生长有着明显的关系 .     

RCN2和PEAK1在结直肠癌中的表达与临床病理特征及预后的关系

目的:检测网织钙结合蛋白2(RCN2)和伪足富集的非典型激酶1(PEAK1)蛋白在结直肠癌组织中的表达情况,分析RCN2和PEAK1表达与患者临床病理特征和预后的关系。方法:免疫组织化学法检测90例结直肠癌组织及其癌旁正常组织中RCN2和PEAK1蛋白表达情况,分析结直肠癌组织RCN2和PEAK1表达与患者临床病理特征的关系,Kaplan-Meier生存曲线分析RCN2和PEAK1表达对患者预后的影响,Spearman等级相关检验结直肠癌组织RCN2和PEAK1表达的相关性。结果:RCN2和PEAK1蛋白在结直肠癌组织中的阳性表达率均明显高于癌旁正常组织(P0.05)。结直肠癌组织RCN2表达与肿瘤直径、浸润深度和TNM分期均有关(P0.05),PEAK1表达与肿瘤浸润深度、淋巴结转移和TNM分期均有关(P0.05)。Log Rank检验结果显示,RCN2阳性表达组和PEAK1阳性表达组患者的术后5年总生存率均分别低于RCN2阴性表达组和PEAK1阴性表达组患者(P0.05)。结直肠癌组织RCN2和PEAK1表达呈正相关性(r=0.586,P=0.000)。结论:RCN2和PEAK1蛋白在结直肠癌组织中呈高表达,且均与肿瘤恶性进展和不良预后关系密切。RCN2和PEAK1可作为结直肠癌治疗靶标的候选分子。     

胃肠道间质瘤中P21 WAF1及Cyclin D1的表达和意义

目的检测P21WAF1及cyclin D1在胃肠道间质瘤（gastrointestinal stromal tumor,GIST）中的表达及分布,并探讨其与GIST的Fletcher分级、有无坏死及转移复发等临床病理学特征之间的关系,分析p21WAF1和cyclin D1在GIST中的作用及其相关性。方法应用免疫组化SP法观察70例手术切除胃肠道间质瘤中P21WAF1及cyclin D1的表达情况。结果P21WAF1和cyclin D1在GIST中阳性表达率分别为34.29%（24/70）和57.14%（40/70）。按Fletcher分级,随着危险程度级别的增高,P21WAF1蛋白阳性表达逐渐减低,cyclin D1蛋白阳性表达逐渐增高,差异有统计学意义。此外,cyclin D1与肿瘤细胞有无坏死及转移复发有关（P〈0.05）,有坏死及转移复发的病例显示cyclin D1高表达率。P21WAF1与cyclin D1在蛋白表达上无相关性（r=-0.165P=0.172）。结论P21WAF1蛋白表达与Fletcher分级相关（P〈0.05）。cyclin D1与Fletcher分级、肿瘤细胞有无坏死及转移复发有关（P〈0.05）。P21WAF1与cyclin D1在蛋白表达上无相关性。P21WAF1和cyclin D1的表达情况能够提示GIST的恶性程度的高低及预后的好坏,与GIST生物学行为密切相关,它们有可能成为判断GIST生物学行为的评价指标。     

结直肠癌相关周期蛋白质研究进展

细胞周期蛋白是调控真核细胞有丝分裂时相的一类蛋白质,在肿瘤细胞的分裂增殖活动中同样起到十分重要的调控作用。在结直肠癌中,细胞周期蛋白的异常表达和调节失控十分常见。在结直肠癌相关周期蛋白的研究中,关于细胞周期蛋白Cyclin D1的研究最深入,可作为结直肠癌的一项诊断指标并作为其增殖程度的监测。近年来,随着周期蛋白Cyclin E、B1和周期蛋白依赖激酶Cdk1、Cdk4以及p21等在结直肠癌发生发展中的作用陆续得到一系列相关实验的初步证实,结直肠癌的研究不断向前推进,细胞周期蛋白必将为结直肠癌的治疗提供新的靶点。本文主要从细胞周期蛋白在结直肠癌中的表达、治疗效果这2个方面,介绍近年来结直肠癌相关周期蛋白的研究进展。     

RNA干扰Ｃyclin D1基因表达对瘢痕疙瘩成纤维细胞增殖和G1期调控的影响

为研究siRNA干扰瘢痕疙瘩成纤维细胞cyclin D1基因表达,对瘢痕疙瘩成纤维细胞的增殖、细胞周期和G1期调控的影响,构建了靶向cyclin D1的siRNA表达质粒.利用LipofecmmineTM2000转染体外培养的瘢痕疙瘩成纤维细胞,应用荧光定量PCR、RT-PCR检测cyclin D1 mRNA的干扰效果,应用MTT法、流式细胞仪检测细胞增殖和细胞周期的变化,应用免疫组织化学染色检测成纤维细胞中cyclin D1、CDK4、P16、pRb蛋白表达的影响.主要结果如F:a.靶向cyclin D1的特异性siRNA序列可以高效地抑制成纤维细胞cyclin D1基因表达,对照组与实验组在mRNA水平其表达抑制率分别为63.68%和92.83%(P<0.01);b.可以显著抑制瘢痕疙瘩成纤维细胞的增殖,改变细胞周期分布,G0/G1期细胞比例显著高于各对照组(P<0.05),细胞分裂被阻滞;c.免疫组化染色发现,转染72 h后,过表达的cyclin D1、CDK4和pRb蛋白,在瘢痕疙瘩成纤维细胞中均出现了不同程度的表达下调,而低表达的P16则呈上调表现.由上述结果可见,构建的靶向cyclin D1的RNAi表达质粒,可有效地抑制瘢痕疙瘩成纤维细胞cyclin D1基因表达,通过改变Gl期相关周期蛋白的水平,影响G1/S期的进程,显著地抑制成纤维细胞的增殖.     

孕激素诱导的microRNA-1a抑制子宫内膜上皮细胞增殖

本文旨在研究孕激素诱导micro RNA-1a(mi R-1a)在子宫内膜上皮细胞(endometrial epithelial cells,EECs)的表达及其对EECs增殖的作用。用雌激素(E2组)或雌、孕激素联合(E2P4组)处理去卵巢小鼠,q PCR检测mi R-1a的成熟体mi R-1a-3p的表达;将mi R-1a-3p拟似剂或抑制剂注入各组小鼠的一侧子宫角,另一侧注入拟似剂或抑制剂对照,流式细胞术检测mi R-1a-3p对EECs细胞周期的影响;免疫组化检测mi R-1a-3p对细胞周期蛋白cyclin D2、cyclin E1和cyclin E2表达的影响。在体外实验,将分离培养的原代小鼠EECs分为两组,分别给予雌激素处理(E2组)和雌、孕激素联合处理(E2P4组),q PCR检测mi R-1a-3p的表达;再用mi R-1a-3p拟似剂作用于雌激素预处理细胞,对照组给予非特异性拟似剂,Ed U掺入实验检测细胞增殖活性。体内q PCR结果显示,E2P4组小鼠EECs mi R-1a-3p的表达量相比E2组明显增加(P0.05)。流式细胞术结果显示mi R-1a-3p拟似剂能够将E2处理细胞的细胞周期进程阻滞在G1/S期(P0.05);mi R-1a-3p抑制剂能够部分逆转P4对细胞周期进程的G1/S期阻滞(P0.05)。小鼠子宫组织免疫组化结果显示mi R-1a-3p拟似剂能较明显地抑制cyclin E1和cyclin E2蛋白的表达(P0.05),而对cyclin D2蛋白表达无影响(P0.05)。体外q PCR结果显示E2处理组和E2P4联合处理组细胞中都未检测到mi R-1a-3p表达,体外Ed U掺入实验表明外源性mi R-1a-3p拟似剂能够一定程度抑制雌激素促细胞增殖作用(P0.05)。以上结果表明,孕激素可通过诱导mi R-1a-3p表达引起细胞周期G1/S期阻滞,从而抑制EECs细胞增殖,这种抑制增殖作用与其抑制cyclin E1和cyclin E2蛋白表达有关。     

siRNA-cyclin D1对乳腺癌MCF-7细胞增殖的抑制作用

研究小干扰RNA(small interfering RNA,siRNA)对乳腺癌MCF-7细胞株cyclin D1表达的抑制及对细胞增殖的影响。化学合成针对cyclin D1基因的siRNA,转染MCF-7细胞株;分别应用荧光定量PCR和免疫印迹测定cyclin D1 mRNA和蛋白的表达,CCK-8测定细胞的增殖活性,流式细胞仪检测细胞周期,软琼脂培养检测细胞克隆形成能力。在实验中,10、50、100 nmol/L siRNA-cyclin D1分别使MCF-7细胞cyclin D1 mRNA表达降低了57．85%、63．22%和68．02%,蛋白表达降低了51．13%、62．09%、77．68%。转染siRNA-cyclin D1后,细胞增殖受到抑制,细胞周期阻滞于G1期,软琼脂克隆形成率降低。结果提示siRNA可以有效抑制MCF-7细胞株中cyclin D1的表达,使细胞周期阻滞于G1期,从而抑制细胞增殖。     

B7H1 Expression and Epithelial-To-Mesenchymal Transition Phenotypes on Colorectal Cancer Stem-Like Cells

Cancer stem cells (CSCs) can invade and metastasize by epithelial-to-mesenchymal transition (EMT). However, how they escape immune surveillance is unclear. B7H1 is crucial negative co-stimulatory molecule but little information about whether it works in CSCs. Therefore, we determined the expression of B7H1 and EMT-associated markers in colorectal cancer stem-like cells to investigate a possible immunoevasion way of CSCs. We enriched CD133⁺ colorectal cancer cells which manifested the CSCs-like properties such as higher levels of other stem cell markers Oct-4 and Sox-2, tumor sphere forming ability and more tumorigenic in NOD/SCID mice. These CD133⁺ cells possess EMT gene expression profile including higher level of Snail, Twist, vimentin, fibronectin and lower level of E-cadherin. Moreover, CD133⁺ cells in both cell line and colorectal cancer tissues expressed high level of negative co-stimulate molecule B7H1. Furthermore, some B7H1⁺ cancer cells also showed the characteristic of EMT, indicating EMT cells could escape immune attack during metastasis. B7H1 expression and EMT phenotypes on CSCs indicates a possible immunoevasion way.     

miR-130b Promotes CD133(+) liver tumor-initiating cell growth and self-renewal via tumor protein 53-induced nuclear protein 1

A novel paradigm in tumor biology suggests that cancer growth is driven by stem-like cells within a tumor, called tumor-initiating cells (TICs) or cancer stem cells (CSCs). Here we describe the identification and characterization of such cells from hepatocellular carcinoma (HCC) using the marker CD133. CD133 accounts for approximately 1.3%-13.6% of the cells in the bulk tumor of human primary HCC samples. When compared with their CD133? counterparts, CD133(+) cells not only possess the preferential ability to form undifferentiated tumor spheroids in vitro but also express an enhanced level of stem cell-associated genes, have a greater ability to form tumors when implanted orthotopically in immunodeficient mice, and can be serially passaged into secondary animal recipients. Xenografts resemble the original human tumor and maintain a similar percentage of tumorigenic CD133(+) cells. Quantitative PCR analysis of 41 separate HCC tissue specimens with follow-up data found that CD133(+) tumor cells were frequently detected at low quantities in HCC, and their presence was also associated with worse overall survival and higher recurrence rates. Subsequent differential microRNA expression profiling of CD133(+) and CD133? cells from human HCC clinical specimens and cell lines identified an overexpression of miR-130b in CD133(+) TICs. Functional studies on miR-130b lentiviral-transduced CD133? cells demonstrated superior resistance to chemotherapeutic agents, enhanced tumorigenicity in vivo, and a greater potential for self renewal. Conversely, antagonizing miR-130b in CD133(+) TICs yielded an opposing effect. The increased miR-130b paralleled the reduced TP53INP1, a known miR-130b target. Silencing TP53INP1 in CD133? cells enhanced both self renewal and tumorigenicity in vivo. Collectively, miR-130b regulates CD133(+) liver TICs, in part, via silencing TP53INP1.     

Is CD133 a biomarker for cancer stem cells of colorectal cancer and brain tumors? A meta-analysis

Background: CD133 has been used to identify normal and cancer stem cells from several different tissues. Nowadays some researchers have reported that CD133 expression was not restricted to cancer stem cells (CSCs) of colorectal cancer and brain tumors, and CD133-negative subsets could also initiate tumors. We therefore performed a meta-analysis to assess the value of CD133 as a biomarker of CSCs for colorectal cancer and brain tumors. Methods: A Medline search was performed to identify relevant studies for the analysis. The meta-analysis was done using RevMan 5.0 software. Outcome measures were colony formation rate and xenotransplanted tumor formation rate. Results: Fifteen identified studies were available for analysis. For in vitro tests, there were no significant differences in the colony formation rates between CD133-positive and CD133-negative cells for colorectal cancer and brain tumors. For in vivo tests, the xenotransplanted tumor formation rate showed a significant difference between CD133-positive cells and CD133-negative cells in colorectal cancer only, corresponding to a risk difference of 0.40 (95%CI: 0.07, 0.73). Samples (cell lines versus tissues), applied biomarkers (combined versus single), and injection site were included as factors in sensitivity analyses, but the results were very inconsistent. Conclusions: CD133 may not be suitable as a universe biomarker in identifying CSCs of colorectal cancer and brain tumors. Additional studies are necessary to further delineate its role.     

肿瘤干细胞标记物CD133与miR-429在大肠癌组织中的表达及其相关性研究

目的：检测CD133不同亚群大肠癌细胞HT-29的miR-429表达情况,探讨miR-429及CD133的表达与肿瘤的发生发展之间的关系。方法：采用荧光活化细胞分选法（FACS）分选出CD133不同亚群细胞,实时荧光定量PCR分别检测两组细胞miR-429的表达,合成miR-429寡核苷酸和阴性对照miRNA并分别转染CD133＋和CD133＋两个亚群细胞。再将细胞种植于非肥胖糖尿病／严重联合免疫缺陷（NOD／SCID）小鼠体内构建移植瘤模型,不同时间测量肿瘤体积和重量,RT—PCR及蛋白质印迹检测CD133＋和CD133＋两组肿瘤CD133mRNA和蛋白质表达。结果：血清检出CD133＋细胞为67．9％,miR-429的表达量是CD133＋细胞的（1．83±0．91）倍（P〈0．05）,CD133＋比例与miR-429表达呈负相关（r=0．591,P〈0．05）;miR-429＋／CD133＋组的移植瘤体积及重量与对照组比较有统计学差异（P〈0．05）,且miR-429＋/CD133＋组成瘤时间较对照组晚约2周,但miR-429＋/CD133＋组的移植瘤CD133表达量低,与阴性对照组比较无明显差异（P〉0．05）。结论：miR-429可能作为CD133的负性调控因子,具有抑制肿瘤生长的作用,但miR-429与CD133在肿瘤发生、发展过程中的作用机制有待进一步研究阐明。     

PDGF-D、MPO与CD15在大肠癌中的表达及临床相关性研究

目的：探讨血小板源性生长因子D（PDGF-D）、髓过氧化物酶（MPO）YL粒细胞相关抗原（CD15）在大肠癌组织中的表达及其与临床特征之间的关系。方法：采用免疫组化染色方法检测88例大肠癌组织、72例大肠腺瘤组织及50例正常大肠粘膜组织中PDGF-D、MPO及CD15的表达情况。结果：PDGF—D、MPO、CD15在大肠癌组织中的阳性表达率分别为85．23％、63．64％、61．36％。PDGF—D、MPO在正常组、大肠腺瘤组和大肠癌组三者之间的表达均有显著性差异（P〈0．05）。CD15在正常组、大肠腺瘤组中的阳性表达率与大肠癌组中的阳性表达率有显著性差异（P〈0．05）,但在正常组与大肠腺瘤组中的阳性表达率无显著性差异（P〉0．05）。PDGF—D、MPO、CD15的表达在有淋巴结转移组织中的阳性率分别为92_31％、75．00％,73．08％;在无淋巴结转移组织中的阳性率分别为75．00％、52．78％,47．22％,三者在有无淋巴结转移组织中的阳性率均有显著性差异（P〈0．05）。PDGF．D、MPO、CD15在大肠癌中的表达与性别、年龄及组织分化程度均无相关（P〉0．05）。经Spearman相关性分析,PDGF—D及MPO在大肠癌的表达具有相关性（P〈O．05）。大肠癌中CD15与PDGF—D、MPO的表达无明显相关性（P〉0．05）：结论：PDGF—D、MPO与CDl5在大肠癌中的高表达,提示均参与了大肠癌的发生发展,可作为大肠癌恶性程度和侵袭转移的分子生物学标志物。     

肿瘤干细胞标记物CD_(133)与miR-429在大肠癌组织中的表达及其相关性研究

目的:检测CD133不同亚群大肠癌细胞HT-29的miR-429表达情况,探讨miR-429及CD133的表达与肿瘤的发生发展之间的关系。方法:采用荧光活化细胞分选法(FACS)分选出CD133不同亚群细胞,实时荧光定量PCR分别检测两组细胞miR-429的表达,合成miR-429寡核苷酸和阴性对照miRNA并分别转染CD133+和CD133-两个亚群细胞。再将细胞种植于非肥胖糖尿病/严重联合免疫缺陷(NOD/SCID)小鼠体内构建移植瘤模型,不同时间测量肿瘤体积和重量,RT-PCR及蛋白质印迹检测CD133+和CD133-两组肿瘤CD133mRNA和蛋白质表达。结果:血清检出CD133+细胞为67.9%,miR-429的表达量是CD133+细胞的(1.83±0.91)倍(P0.05),CD133+比例与miR-429表达呈负相关(r=0.591,P0.05);miR-429+/CD133+组的移植瘤体积及重量与对照组比较有统计学差异(P0.05),且miR-429+/CD133+组成瘤时间较对照组晚约2周,但miR-429+/CD133+组的移植瘤CD133表达量低,与阴性对照组比较无明显差异(P0.05)。结论:miR-429可能作为CD133的负性调控因子,具有抑制肿瘤生长的作用,但miR-429与CD133在肿瘤发生、发展过程中的作用机制有待进一步研究阐明。     

Augmented CD133 expression in distal margin correlates with poor prognosis in colorectal cancer

Pathological assessment of excised tumour and surgical margins in colorectal cancer (CRC) play crucial role in prognosis after surgery. Molecular assessment of margins could be more sensitive and informative than conventional histopathological analysis. Considering this view, we evaluated the distal surgical margins for expression of cancer stem cell (CSC) markers. Cellular and molecular assessment of normal, tumour and distal margin tissues were performed by flow cytometry, real‐time q‐PCR and immuno‐histochemical analysis for CRC patients after tumour excision. CRC patients were evaluated for expression of CSC markers in their normal, tumour and distal tissues. Flow cytometry assay revealed CD133 and CD44 enriched cells in distal margin and tumour compared to normal colorectal tissues, which was further confirmed by immunohistochemistry. Most importantly, immunohistochemistry also revealed the enrichment of CSC markers expression in pathologically negative distal margins. Patients with distal margin enriched for CD133 expression showed an increased recurrence rate and decreased disease‐free survival. This study proposes that although distal margin seems to be tumour free in conventional histopathological analysis, it could harbour cells enriched for CSC markers. Further CD133 could be a promising molecule to be used in molecular pathology for disease prognosis after surgery in CRC patients.     

人白细胞抗原G在结直肠癌中的表达及意义

目的：在蛋白水平检测人白细胞抗原G（HLA-G）在结直肠癌组织中的表达,探讨HLA-G分子在结直肠癌不同分级和不同分期中的表达差异及在肿瘤逃逸中作用。方法：用免疫组织化学法检测结直肠癌和癌旁正常结直肠组织HLA-G的表达情况,用SPSS13.0软件、Kruskal-Wallis test进行分析。结果：HLA-G分子在结直肠癌组织中的表达率为42.3%（41/97）,在癌旁正常结直肠组织的表达率为0（0/20）;HLA-G分子表达与结直肠癌临床TNM分期（P〈0.05）和组织学分级（P〈0.01）相关。结论：HLA-G分子在结直肠癌组织中表达上调,且与结直肠癌的侵袭性生长密切相关;HLA-G分子可能下调宿主对肿瘤细胞的免疫应答反应,使肿瘤细胞逃避机体的免疫监视。     

Cyclin B1 Suppresses Colorectal Cancer Invasion and Metastasis by Regulating E-Cadherin

Cyclin B1, a mitotic cyclin, has been implicated in malignances. However, its contribution to colorectal cancer invasion and metastasis are still not well understood. Here, we demonstrated that the invasion and metastasis of colorectal cancer is regulated by Cyclin B1. Overexpression of Cyclin B1 was observed in colorectal cancer tissues, but this elevated expression was negatively associated with lymph node metastasis, distant metastasis stage, and TNM stage. The Kaplan-Meier survival analysis proved that low Cyclin B1 expression was associated with poor overall survival of patients with colorectal cancer. Inhibition of Cyclin B1 in colorectal cancer cells enhanced the cell migration and invasion of three different colorectal cancer cell lines. In studying the possible mechanism by which Cyclin B1 suppresses colorectal cancer invasion and metastasis, we observed that suppression of Cyclin B1 decreased the expression of E-cadherin protein level. Our findings suggest that Cyclin B1 could suppress the invasion and metastasis of colorectal cancer cells through regulating E-cadherin expression, which enables the development of potential intervention strategies for colorectal cancer.