贲门腺癌中E-钙黏蛋白基因甲基化状态研究

目的：研究贲门腺癌（gastric cardiac adenocarcinoma，GCA）中E-钙黏蛋白（E—cadherin）的基因甲基化状态及其蛋白表达情况。方法：分别应用巢式甲基化特异性PCR（methylation specific PCR，MSP）方法及免疫组织化学SP法检测贲门癌组织及相应癌旁组织的甲基化和蛋白表达情况。结果：92例贲门癌组织中有63例E—cadherin发生了甲基化，甲基化率为68．5％，显著高于癌旁正常组织（P〈0．001）；Ⅲ期和Ⅳ期的发生率明显高于Ⅰ期和Ⅱ期患者（P=0．01）；低分化腺癌组发生甲基化的比率显著高于中、高分化腺癌组（P〈0．01）。92例贲门癌组织中有51例蛋白表达呈明显的异质性．贲门癌组织的E-cadherin蛋白表达率为44．6％，与相应癌旁正常组织相比差异有统计学意义（P〈0．001）。Ⅲ期和Ⅳ期患者的蛋白表达明显低于Ⅰ期和Ⅱ期患者（P〈0．01）；低分化腺癌组的蛋白表达率也低于中、高分化腺癌组，差异有统计学意义（P〈0．05）。结论：E—cadherin基因启动子区发生甲基化导致的基因沉默可能是贲门腺癌发生的机制之一，可作为反映贲门腺癌生物学行为的指标。     

血清胃泌素放射免疫测定在贲门癌的临床应用

本文采用放射免疫测定技术对３５例贲门癌病人及３０例正常人空腹进行了血清胃泌素浓度的检测，结果贲门癌病人空腹血清胃泌素水平（１９１．４±４６．３Ｐｇ／ｍｌ）显著高于正常对照组（４８．３±２４．９Ｐｇ／ｍｌ）；有淋巴结转移者（１０７．３±４０．６Ｐｇ／ｍｌ）显著高于无淋巴结转移者（４９．３±３１．６Ｐｇ／ｍｌ）；癌肿浸润粘膜肌层以外者（１１３．７±４１．３Ｐｇ／ｍｌ）显著高于癌肿浸润粘膜肌层以内者（６２．８±３７．１Ｐｇ／ｍｌ）；分化良好的腺癌病人（９２．４±４３．８Ｐｇ／ｍｌ）较低分化腺癌病人（１０９．４±５１．３Ｐｇ／ｍｌ）无显著差异性。研究结果表明：空腹血清胃泌素测定有助于探讨胃泌素与贲门癌的关系、诊断以及预后的判断。     

MGMT在结直肠癌中表达的临床病理意义

目的：探讨大肠癌MGMT表达的临床病理意义。方法：采用免疫组织化学法检测139例大肠癌组织及48例正常大肠组织巾的MGMT表达，分析其与临床病理参数的相关性。结果：MGMT在大肠癌组织中的阳性表达率为75．5％（105／139），明显高于正常大肠组织的12．5％（6／48）（P=0．000）；大肠癌组织中，MGMT的阳性表达率在浸润达浆膜组为82．0％（82／100），明显高于未达浆膜组的58．9％（23／39）（P=0．005）；在低分化组为33．3％（9／27），明显低于高分化组和中分化组的78．1％（32／41）和90．0％（64／71）（P=0．000）；但与患者性别、年龄、肿瘤发生部位、淋巴转移及Dukes分期均无明显相关性（P均〉0．05）。结论：监控MGMT表达可有助于大肠癌的诊断和预后判断。     

子宫内膜腺癌中孕激素依赖的cyclinG1与PRA／PRB表达的相关性及临床意义

目的：探讨孕激素依赖的cyclinG1与孕激素受体亚型PRA和PRB在子宫内膜腺癌中表达的相关性及cyclinG1在子宫内膜腺癌中低表达的原因。方法：采用免疫组化sP法分别检测48例子宫内膜腺癌组织标本（高分化腺癌17例,中分化腺癌19例,低分化腺癌12例）中cyclinG1与PRA、PRB蛋白的表达,显微镜下计数阳性细胞百分数,以5％作为判断标本阳性表达的标准,同时用BI2000图像分析系统测定灰度值反映蛋白表达水平,分析在不同分化程度的子宫内膜腺癌中PRA、PRB和cyelinG1表达的差异及其与子宫内膜腺癌病理分级的关系,同时分析cyclinG1表达与PRA、PRB的相关性。结果：48例高、中、低分化子宫内膜腺癌中,PRA阳性表达分别为88．2％（15／17）、79．0％（15／19）、66．7％（8／12）,PRA的表达与病理分级无关联性（P〉0．05）;PRB阳性表达分别为47．1％（8／17）、15．8％（3／19）、8．3％（1／12）,cyclinG1阳性表达分别为35．3％（6／17）、10．5％（2／19）、0％（0／12）,PRB和cyclinG1的表达与病理分级有关联性（P〈0．05）,即随分化程度降低而明显降低;cyclinG1表达与PRB表达有关联性（P〈0．05）,与PRA的表达无关联性。结论：子宫内膜腺癌中PRB和cyelinG1的表达具有关联性,都随肿瘤分化程度降低而降低。子宫内膜腺癌中PRB低表达可能是导致cyclinG1低表达的原因之一。     

贲门腺癌雌孕激素受体及PCNA表达相关性初探

目的：比较贲门腺癌增殖细胞核抗原(proliferating cell nuclear antigern,PCNA)及雌激素受体(ER)、孕激素受体(PR)检测结果，探讨PCNA及ER、PR与贲门癌发生发展和预后的关系。方法：应用免疫组化法对66例贲门癌进行PCNA和ER、PR检测。结果：高分化腺癌PCNA阳性率高，ER、PR低；低分化腺癌PCNA阳性率低，ER、PR高。说明PCNA、ER、PR表达与肿瘤分化程度有相关性(P＜0．05)。结论：ER、PR、PCNA与贲门癌发生、发展有关，可能是反映贲门癌生物学行为和预测预后的重要指标。其检测具有实际临床意义，对临床治疗有参考价值。     

胃癌组织中肥大细胞与C－erbB－2癌基因蛋白

用俾士麦棕法和免疫组织化学方法检测了５７例胃癌组织中肥大细胞（ＭＣ）和Ｃ－ｅｒｂＢ－２癌基因蛋白。结果表明：（１）ＭＣ计数与胃癌的分化程度和转移有关，高、中分化腺癌高于低分化腺癌和未分化癌（Ｐ＜０．０５），无转移者高于有转移者（Ｐ＜０．０５）；（２）Ｃ－ｅｒｂＢ－２癌基因蛋白阳性表达与胃癌的分化程度和转移无关（Ｐ＞０．０５）；（３）Ｃ－ｅｒｂＢ－２癌基因蛋白阳性表达与ＭＣ计数有关，ＭＣ高计组，Ｃ－ｅｒｂＢ２癌基因蛋白阳性表达低于ＭＣ低计组（Ｐ＜０．０５）。     

增殖细胞核抗原在胃癌中的表达

本文应用抗增殖细胞核抗原的单克隆抗体ＰＣ１０，用ＬＳＡＢ免疫组化方法对４０例胃癌标本进行研究。结果发现：胃癌不同分化程度各组中ＰＣＮＡ指数存在差异（Ｐ＜０．０２），低分化腺癌＞中分化腺癌＞高分化腺癌；淋巴结癌转移阳性组ＰＣＮＡ指数显著高于无淋巴结转移组（Ｐ＜０．０５）；癌细胞浸润达肌层、浆膜层者ＰＣＮＡ指数显著高于粘膜内癌（Ｐ＜０．０１）。结果显示：此方法是在石蜡切片上检测胃癌增殖指数的一个有效手段，并对判断胃癌患者的预后有一定作用。     

蛋白质飞行质谱技术在原发性肝癌诊断中的应用

目的研究原发性肝癌患者与健康人血清蛋白质表达的差异性,寻找对原发性肝癌更有效的肿瘤诊断标志物。方法应用表面增强激光解析电离飞行时间质谱（SELDI—TOF—MS）技术检测50例原发性肝癌患者、50名健康对照者血清中的蛋白质谱,寻找有意义的蛋白质谱。同时采用双抗体夹心法检测血清甲胎蛋白（AFP）。结果原发性肝癌患者血清4个蛋白质峰与健康对照组比较差异有统计学意义。分别为：3354．71,8825．80（高表达）,4345．08,13715．01（低表达）。从中筛选出质荷比（M／z）分别为3354．71、8825．80差别最显著的蛋白质峰,使用这两个蛋白质峰作为原发性肝癌的诊断模式,其灵敏度、特异度分别为90％（45／50）,94％（47／50）。100例患者中,AFP阳性27例,灵敏度为54％（27／50）,特异度为100％（30／30）。结论SELDI—TOF—MS蛋白质芯片技术在原发性肝癌的诊断及肿瘤特异性蛋白质生物标志的筛选中具有一定的价值,灵敏度和特异度较高,操作简单,正确诊断指数（r=83）优于AFP（r=53）。     

食管贲门癌血液胃动素和胃泌素的变化及意义

作者采用放免法测定了５９例食管贲门癌患者和３０例健康人血液中胃动素和胃泌素的含量。结果表明：食管贲门癌患者血浆胃动素含量显著高于健康人（Ｐ＜０．０５），且病期越晚，胃动素含量越高，血清胃泌素含量与健康人相比无显著差异（Ｐ＞０．０５），病期越晚，胃泌素含量越低。上述自动素和胃泌素的变化对食管贲门癌病期的判断有重要的参考价值。血清胃泌素测定对贲门癌术前选择治疗方法可提供参考依据，     

贲门癌术前大剂量放疗与单纯手术的临床研究

1987年3月至1991年10月对66例贲门癌随机分组治疗，术前放疗和单纯手术各33例。术前放疗组在术前接受照射5天，共5次25Gy后，体息1～3周后手术，观察术中出血量、手术时间、术中输血量、术后并发症、创口愈合情况，其结果与单纯手术组相同．术前放疗组切除率为88％（29／33），单纯手术组为70％（23／33），P＜0．05．近期疗效术前放疗组1年、3年生存率为76％（25／33）、48％（16／33），而单纯手术组为52％（17／33）、24％（8／33），呈显著性差异。两组5年生存率各为21％（6／28）与14％（4／28），P＞0．05，无统计学意义．提示术前大剂量放方能提高贲门癌手术切除率和近期疗效．     

Small-cell carcinoma of the gallbladder - a clinicopathological, immunohistochemical and flow cytometric study of 15 cases

Small cell carcinoma (SC) of the gallbladder is an uncommon tumor, and not enough information of this tumor has been previously reported. The SCs in this series occured in nine women and six men (mean age; 64.5 years). Histologically, they consisted of small atypical cells with scanty cytoplasm, hyperchromatic nuclei and inconspicuous nucleoli growing in sheets and cords. Two tumors contained neoplastic glands similar to those of well-differentiated adenocarcinoma and a histological transition between SC and adenocarcinoma was seen in one of the two tumors. Argyrophil granules were present in 10 tumors. The tumor cells were immunoreactive to epithelial markers (epithelial membrane antigen: 12/14; AE1/AE3: 12/14; CAM 5.2: 9/14; carcinoembryonic antigen: 7/14) and neuroendocrine markers (neuron specific enolase: 11/14; chromagranin A: 4/14; Leu 7: 10/14; adrenocorticotrophic hormone: 6/14). Abnormalities in tumor suppressor gene p53 expression were found in 9 of 14 SCs by using monoclonal antibody PAb 1801. Flow cytometry revealed aneuploidy in 7 (78%) of 9 in the SC and 26 (40%) of 65 in the adenocarcinoma. The survival curve of the SCs was less favorable than that of papillary adenocarcinoma and well differentiated adenocarcinoma in pTNM stage 2-4 (P=0.0027, P=0.0017, respectively). These results suggested that the SCs of the gallbladder arose from common primitive cells capable of endocrine and epithelial differentiation, while most SCs (78%) showed DNA aneuploid by flow cytometry and their prognosis was worse than that of differentiated adenocarcinoma of the gallbladder.     

Identification and validation of S100A7 associated with lung squamous cell carcinoma metastasis to brain

To identify potential markers associated with non-small cell lung cancer (NSCLC) metastasis to brain, comparative proteome analysis on two lung squamous cell carcinoma (SCC) cell lines, NCI-H226 and H226Br (the brain metastatic cell line of NCI-H226), was performed using two-dimensional electrophoresis (2-DE) followed by a tandem mass spectrometer with a matrix-assisted laser desorption/ionization (MALDI) source. Twenty differential proteins were identified, of which 6 proteins were up-regulated in H226Br cell compared with NCI-H226 cells, whereas 14 proteins were down-regulated. S100A7 and 14-3-3sigma, two of candidate proteins significantly upregulated and downregulated in H226Br cell, were selected to verify the liability of the differential proteins by Western blot. The results were in accordance with 2-D data. To determine whether S100A7 overexpression is actually associated with SCC metastasis to brain, S100A7 protein was testified in 10 brain metastasis tissues from NSCLC, 38 primary NSCLC tissues including half matched local positive lymph nodes, 5 primary brain tumors and 2 non-cancer brain tissues by immunohistochemistry. Of particular interest to us was that the positive staining of S100A7 could be found in 3/5 (60%) brain metastases tissue from SCC and 8/21 (38%) the primary lung SCC tissues, while no positive staining was observed in the brain metastases tissue from Ad (n=5), the primary adenocarcinoma (Ad) tissues (n=17), the primary brain tumors (n=5), all local positive lymph nodes from the primary NSCLC (n=19) and non-cancer brain tissues (n=2). These findings suggest that S100A7 expression is closely associated with SCC metastasis to brain and may be a potential biomarker for monitoring the development of SCC.     

NDRG2基因在贲门腺癌中的甲基化状态及表达

目的： 探讨贲门腺癌(GCA)中NDRG2(N-myc downstream-regulated gene 2)基因启动子区的甲基化状态,并分析其甲基化与表达之间的相关性。方法：应用甲基化特异性PCR(MSP)方法检测97例贲门腺癌组织及相应癌旁组织中NDRG2基因的甲基化状态,应用RT-PCR和免疫组织化学方法检测97例贲门腺癌组织及相应癌旁组织中NDRG2的mRNA和蛋白表达情况。结果：NDRG2基因启动子区在贲门腺癌组织中的甲基化率(49.5%)显著高于癌旁正常组织(5.1%)(P<0.05),且Ⅲ期和Ⅳ期贲门腺癌患者中NDRG2基因甲基化的比率显著高于Ⅰ期和Ⅱ期患者,低分化组中NDRG2基因发生甲基化的比率显著高于高中分化组。贲门腺癌组织中NDRG2 mRNA表达水平显著低于癌旁正常组织(P<0.05)。贲门腺癌组织中NDRG2蛋白表达阳性率为44.3%(43/97),显著低于相应癌旁正常组织的蛋白表达94.8%(92/97)(P<0.01),且贲门腺癌组织中NDRG2蛋白表达缺失与其启动子区的甲基化有明显的相关性(r=-0.510,P<0.01)。结论：NDRG2基因启动子区的高甲基化导致的基因沉默可能是贲门腺癌中此基因表达降低的机制之一。     

Isobaric tags for relative and absolute quantitation-based proteomics analysis of the effect of ginger oil on bisphenol A-induced breast cancer cell proliferation

Several chemicals in the environment, particularly those with estrogenic activity and small amounts (micromolar or lower) of environmental estrogen can cause changes in cell function and interfere with endocrine functions of animals and humans. These compounds enter the human body and increase the load of estrogen in the body, leading to an increasing incidence of estrogen-related tumors in breast cancer, ovarian cancer and endometrial cancer. Previous studies have demonstrated that ginger can inhibit the expression of estrogen receptors, while the bioactive ingredients of ginger sig-nificantly inhibit proliferation and promote the apoptosis of breast cancer cells. In the present study, a quantitative proteomics technique based on relative and absolute quanti-tative isobaric labeling was used to determine the effect of ginger essential oil (GEO) and BPA combined treatment on the proteomic characteristics of MCF-7 cells. In total, 5,084 proteins were detected. Proteins that were upregulated >1.2-fold and downregu-lated by >0.8-fold were differentially expressed. Overall, 528 differentially expressed proteins were identified. Compared with the control group, MCF-7 cells treated with GEO, BPA and GEO-BPA resulted in 45 (14 up- and 31 downregulated), 481 (141 up- and 340 downregulated) and 34 (13 up- and 21 downregulated) differentially ex-pressed proteins, respectively. Compared with the BPA group, MCF- 7 cells treated with GEO-BPA resulted in 210 (117 up- and 93 downregulated) differentially expressed proteins, among the 210 differentially expressed proteins in the GEO-BPA group, 10 proteins were associated with oxidative phosphorylation pathways, while succinate dehydrogenase (ubiquinone) iron-sulfur subunit (SDHB), succinate dehydrogenase cytochrome b560 subunit, mitochondrial (SDHC), cytochrome c oxidase subunit 2 and superoxide dismutase (Mn), mitochondrial (SOD2) expression was decreased with GEO-BPA combined treatment. Through the analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, the cellular localization, functional annotation and biological pathways of differentially expressed proteins were ex-amined. The results indicated that GEO-BPA may act through the oxidative phosphory-lation pathway, decreased the expression of SDHB and SDHC, affected the tricarbox-ylic acid cycle and decreased the expression of SOD2. This may have led to oxidative stress and the death of breast cancer cells, and the SDH signaling pathway may be an important mediator of the inhibitory effects of GEO in MCF-7 breast cancer cells. GEO can inhibit the proliferation of breast cancer MCF-7 cells induced by BPA, and the underlying mechanism may be associated with oxidative phosphorylation. These results may aid the development of future treatment strategies for breast cancer caused by environmental estrogen exposure.     

人大肠腺瘤和腺癌之间相关差异蛋白的蛋白质组学研究

目的　应用蛋白质组学的方法,建立人大肠腺癌组织、大肠腺瘤组织、正常大肠黏膜组织的二维电泳图谱,筛选并鉴定三者之间的差异蛋白,发现人大肠癌的潜在生物学标志物。方法　收集同时患有大肠腺瘤的大肠腺癌患者１０例,术前及术后病理证实均为Ｄｕｋｅｓ’Ｂ期。取同一患者术后大肠癌组织、距大肠癌组织１５ｃｍ以上正常大肠黏膜组织以及肠镜下切除大肠腺瘤组织,提取不同组织总蛋白进行二维电泳,用ＩｍａｇｅＭａｓｔｅｒ２ＤＰｌａｔｉｎｕｍ５.０凝胶图像分析软件对双向电泳图依次进行凝胶点的检测、背景消减和编号。识别不同组织之间的差异蛋白点,对差异蛋白点用胶内酶解后行质谱分析和网上数据库鉴定。结果　大肠腺癌组织、大肠腺瘤组织和正常大肠黏膜组织之间存在９０个差异蛋白点。对这些差异点进行质谱分析,经数据库鉴定出７１个蛋白质。经分析,大肠腺瘤组织与正常大肠黏膜组织相比,１７个蛋白表达上调,９个蛋白表达下调;大肠腺癌组织与正常大肠黏膜组织比较,４７个蛋白表达上调,１２个蛋白表达下调;大肠腺癌组织与大肠腺瘤组织相比,３５个蛋白表达上调,８个蛋白表达下调。结论　大肠腺癌组织、大肠腺瘤组织和正常大肠黏膜组织之间存在差异蛋白表达,可能与大肠腺癌的发生发展有关;应用蛋白质组学方法筛选人大肠腺癌发生发展相关蛋白是可行的。     

Gastric atrophy and risk of oesophageal cancer and gastric cardia adenocarcinoma—a systematic review and meta-analysis

BackgroundSeveral studies have reported an association between gastric atrophy and upper gastrointestinal cancers. Our aim was to summarise the available information and calculate the relative risks (RRs) associated with gastric atrophy for gastric cardia adenocarcinoma (GCA), oesophageal squamous cell carcinoma (OSCC), and oesophageal adenocarcinoma (OAC) by conducting a systematic review and meta-analysis.MethodsWe searched the PubMed and ISI-Web of Science databases, as well as the reference lists of the relevant articles. Summary RRs and 95% confidence intervals (95% CI) were calculated using random-effects models for the association between gastric atrophy, defined histologically or by serum pepsinogen markers, and OSCC, OAC, and GCA.ResultsEighteen articles were included in the meta-analysis; 13, 7, and 3 studies reported on GCA, OSCC, and OAC, respectively. The overall RRs (95% CI) for the three cancer types were: GCA, 2.89 (2.09–3.98); OSCC, 1.94 (1.48–2.55); OAC, 0.51 (0.19–1.37). Several subgroup analyses showed the robustness of the results. In the majority of the analyses, there was low to moderate heterogeneity.ConclusionsThis study found two- to threefold increased risk of OSCC and GCA but a possible reduced risk of OAC in people with gastric atrophy. Further studies are needed to establish the association with OAC and causal association with OSCC, and mechanisms of the increased risk need to be investigated for GCA.     

高龄梗阻性结直肠癌的外科治疗

目的:探讨影响70岁以上高龄结直肠癌伴肠梗阻患者的外科治疗及预后因素。方法:回顾性分析中国医学科学院肿瘤医院腹部外科1992年1 月至2001年12月间收治的31例70岁以上高龄梗阻性结直肠癌患者的临床病理资料。采用Kaplan-Meier 法进行生存分析,Log-rank 检验进行统计学比较;应用Cox 比例风险模型进行多因素分析,对外科治疗及影响预后的因素进行分析。结果:全组患者中位年龄74岁,手术后并发症者7 例（22.6%）,手术后30天内死亡2 例（6.5%）。 病理类型分别为管状腺癌28例（高分化5 例,中分化16例,低分化7 例）,黏液腺癌3 例。肿瘤Dukes分期B 期8 例,C 期9 例,D 期14例。全组5 年生存率为22.7% 。行根治性手术组的5 年生存率为44.4% ,非根治手术组的5 年的总体生存率为7.7% 。全组的中位生存期为12个月,根治性手术组的中位生存期38个月,非根治组的中位生存期9 个月。单因素分析显示:高龄、合并症、术前CEA 、术前低蛋白血症、手术时间、根治性手术、分期与预后相关。多因素分析表明高龄、术前低蛋白血症为影响老年梗阻性结直肠癌预后的独立因素。结论:高龄梗阻性结直肠癌患者行根治性切除术预后较好,年龄、术前低蛋白血症是影响其预后的独立因素。      

p16基因C540G和C580T多态与高发区食管癌和贲门癌发病风险的关联

目的探讨p16基因第3外显子3’端非编码区C540G和C580T两个单核苷酸多态与河北省高发区食管鳞状细胞癌（ESCC）和贲门腺癌（GCA）遗传易感性的关系。方法采用聚合酶链反应-限制性片段长度多态性（PCR—RFLP）方法分析265例ESCC患者、238例CA;A患者和246名健康对照的p16基因C540G和C580T多态位点的基因型。结果p16基因C540G三种基因型（C／C、C／G、G／G）的频率分布在ESCC、GCA患者和对照组相比均无显著差异;p16基因C580T三种基因型（C／C、C／T、T／T）的频率在对照组和ESCC、GCA患者组间也无显著差异（P均〉0．05）。单体型分析显示,对照组540C／580C、540C／580T、540G／580C和540G／580T单体型的频率分别为80．1％、10．4％、8．5％和1．0％,ESCC组单体型频率（80．8％、9．6％、8．7％和0．9％）和GCA组的单体型频率（80．2％、9．2％、9．5％和1．1％）与之相比均无显著差异（P均〉0．05）。结论p16基因C540G和C580T多态可能与河北省高发区ES-CC和GCA的易感性无关。     

肺癌缺氧A549细胞的microRNA芯片表达谱分析

目的:研究缺氧对肺腺癌A549细胞中microRNA表达谱的影响,分析靶基因参与的生物学功能和通路。方法:基于miRNA芯片技术和生物信息学分析方法,分析缺氧条件和正常氧条件下培养的A549细胞中差异表达的miRNA,并预测这些miRNA的靶基因,分析靶基因参与的生物学功能和通路。结果:本研究共筛选出14个差异表达miRNA,包括9个在缺氧细胞中上调miRNA和5个下调miRNA。上调和下调miRNA的靶基因都参与DNA转录、核染色质修饰等功能,并且都参与Wnt信号、TGF-β信号和MAPK信号通路。结论:缺氧的肺腺癌A549细胞中miRNA表达谱发生了显著改变,差异表达miRNA对某些基因具有调控作用。     

CENPF通过上调ACKR3/CXCR7促进非小细胞肺癌EMT的研究

目的 探讨CENPF在非小细胞肺腺癌（LUAD）中的表达与患者临床预后的关系及其对肺腺癌细胞转移能力的影响。方法 公共数据库分析CENPF在LUAD中的表达及其与患者预后的关系。免疫组织化学染色验证CENPF LUAD在组织芯片中的表达,Kaplan-Meier分析CENPF表达与肺腺癌患者预后的关系;Cox生存风险比例回归模型分析影响患者生存的因素;卡方分析CENPF表达与患者临床病理分期及分级的关系。慢病毒敲除NCI-H2126细胞中CENPF的表达,检测细胞增殖、侵袭及迁移能力的变化。RNA-seq检测CENPF敲除后细胞mRNA表达谱改变,生物信息学分析CENPF下游信号通路及靶基因,Western blot验证下游基因表达水平变化。结果 CENPF在LUAD肿瘤组织中显著上调（P<0.05）,与病理分期显著相关（P=0.013）,表达越高患者预后越差（P=0.01, P=0.027）。敲除CENPF表达后,细胞增殖、迁移及侵袭能力均显著降低（P<0.01）;RNA-seq富集分析显示细胞趋化因子通路基因表达改变富集显著（P<0.001）;聚类差异分析则表明,ACKR3/CXCR7及CDH2/N-cadherin显著下调,CDH1/E-cadherin则显著上调;Western blot结果证实,敲除CENPF后,ACKR3/CXCR7及N-cadherin显著下调, E-cadherin则显著上调。结论 CENPF的表达与LUAD患者临床预后呈负相关,其通过ACKR3/CXCR7调控与EMT相关的N-cadherin及E-cadherin的表达促进EMT的发生。