Pathogenesis of chronic enteropathy associated with the SLCO2A1 gene:Hypotheses and conundrums

Chronic enteropathy associated with the SLCO2A1 gene(CEAS)is a complex gastroenterological condition characterized by multiple ulcers in the small intestine with chronic bleeding and protein loss.This review explores the potential mechanisms underlying the pathogenesis of CEAS,focusing on the role of SLCO2A1-encoded prostaglandin transporter OATP2A1 and its impact on prostaglandin E2(PGE2)levels.Studies have suggested that elevated PGE2 levels contribute to mucosal damage,inflammation,and disruption of the intestinal barrier.The effects of PGE2 on macrophage activation and Maxi-Cl channel functionality,as well as its interaction with nonsteroidal anti-inflammatory drugs play crucial roles in the progression of CEAS.Understanding the balance between its protective and pro-inflammatory effects and the complex interactions within the gastrointestinal tract can shed light on potential therapeutic targets for CEAS and guide the development of novel,targeted therapies.

SULT1E1蛋白表达和性激素含量与子宫肌瘤发病的相关性研究

目的:探讨性激素及人雌激素硫酸基转移酶在子宫肌瘤发生、发展中的作用。方法:化学发光分析法测定30例子宫肌瘤患者和30例同年龄段健康女性血清及组织匀浆中E2、P、T含量。免疫组化染色法检测SULT1E1蛋白的表达。结果:肌瘤组血清E2含量明显低于健康女性组(P<0.05),其T含量则明显高于健康女性组(P<0.05),P含量各组无显著差异;肌瘤组织匀浆中E2含量显著高于肌瘤包膜外肌层组织(P<0.01),其P、T含量两组间无显著差异;肌瘤组织中SULT1E1蛋白表达与肌瘤包膜外肌层组织比较差异显著(P<0.05),肌瘤组织与肌瘤包膜外肌层组织中SULT1E1蛋白定量表达与相应组织匀浆中E2含量分别呈负相关(r=-0.533,r=-0.498,P<0.01)。结论:子宫肌瘤的发生、发展与子宫肌瘤组织局部SULT1E1酶活性降低有关。

SULT1E1、ERβ在子宫内膜腺癌组织中的表达及其相关性

目的:探讨SULT1E1及ERβ蛋白与子宫内膜腺癌的发生、发展之间的关系。方法:采用Western blot方法检测正常增生期子宫内膜组织、不典型增生子宫内膜组织及子宫内膜腺癌组织中SULT1E1和ERβ蛋白的表达含量。结果:SULT1E1和ERβ蛋白在正常增生期子宫内膜组织、不典型增生子宫内膜组织及子宫内膜腺癌组织中的表达含量逐渐降低,三者比较差异有统计学意义(P<0.05)。不典型增生子宫内膜组织及子宫内膜腺癌组织与正常增生期子宫内膜组织比较差异均有统计学意义(P<0.05)。SULT1E1和ERβ蛋白与子宫内膜腺癌组织学分级、肌层浸润深度、手术病理分期及淋巴结转移等无关(P>0.05)。在子宫内膜腺癌组织中,SULT1E1蛋白与ERβ蛋白表达呈明显正相关(r=0.66,P<0.01)。在正常增生期和不典型增生子宫内膜组织中,SULT1E1蛋白与ERβ蛋白表达无明显相关性(r=0.035,P>0.05;r=0.466,P>0.05)。结论:在子宫内膜腺癌的渐近演变过程中,SULT1E1、ERβ表达降低或缺失可能与子宫内膜癌的早期形成有一定的关系,ERβ蛋白含量越多,SULT1E1蛋白对雌激素的调节作用越强,但不能作为子宫内膜腺癌病情严重程度和预后进行评价的指标。

Tissue expression and immunolocalization of cellular repressor of E1A-stimulated gene in postinfarction dysfunctional myocardium

Background Cellular Repressor of E1A-stimu-lated gene(CREG) is widely expressed in adult tissues such as the brain,heart,lung,liver,intestine and kidney in mice.It is not known whether tissue CREG is decreased in the common setting of myocardial infarction which may lead to heart failure.We studied the expression and protein localization of CREG and its main receptor(IFR2R) in a mouse model of myocardial infarction.Methods Male mice were randomized to proximal left anterior descending ligation.The animals were killed on day 1,3,7,14,and 28 after ligation to examine gene expression and protein production of CREG and IGF2R from the infarct,peri-infarct,and contralateral zones of infarcted heart.Results There was decreased CREG mRNA production throughout the myocardium at dav 1,and the expression gradually increased at day 28 after myocardial infarction.The decreased expression of this glycoprotein was not confined strictly to the infarct or peri-infarct zones but also expressed by cardiac myocytes within the myocardium in the contralateral normal zone.Levels of CREG protein in the infarct and peri-infarct zones declined to 1/3- to 1/2-fold of normal levels and declined to 1/2- to 2/3- fold in the contralateral zone.Finally,the expression of the IGF2R mRNA transcripts was downregulated at day 3 and 7 after ligation in the infarct and peri-infarct zones,suggesting that the signal transduction pathways necessary for CREG in the heart remain intact as CREG biosynthesis decreases. Conclusions CREG is constantly present in a model of large myocardial infarction and is decreased at the early stage within the myocardium.The decreased expression of this glycoprotein is not only confined strictly to the infarct or periinfarct zone but also is expressed by cardiac myocytes within the myocardium contralateral to the infarct.Therefore CREG production decreased due to myocardial stress response to injury.

Lack of association between cellular repressor of E1A-stimulated genes(GREG)polymorphisms and coronary artery disease in the Han population of North China

Objectives Phenotypic switching of smooth muscle cells(SMCs) plays a critical role in the pathogenesis of atherosclerotic lesions such as coronary artery disease (CAD).Accumulating evidence demonstrates(hat a cellular repressor of E1A-stimulated genes(CREG) plays a role in the maintenance of the mature phenotype of vascular SMCs. The purpose of the present study was to assess the possible association between CREG and CAD in the Han population of North China.Methods The promoter region of CREG by direct sequencing was conducted in 48 subjects.Then SNP rs2995073 and another 4 tagSNPs(rs4657669,rs3767443, rsl6859185,rs3753921) were selected for the association study.All five selected SNPs were determined in 1161 patients with angiographically proven CAD and 960 controls with normal coronary angiograms to investigate the possible involvement of CREG in CAD.Results Genotype frequencies of the five examined polymorphisms were similarly distributed between CAD group and controls(P】0.05).Further haplotype analysis also found no significant differences in the distributions between CAD group and controls(P】0.05). Conclusions This study did not show an association between common variants of CREG and CAD in the northern Chinese Han population.

Role of CYP2E1 gene polymorphisms association with hepatitis risk in Northeast India

AIM:To investigate hepatitis virus, genetic and environmental factors, and their interactions in predisposing patients to liver diseases in Northeast India. METHODS:A total of 104 jaundice patients and 124 community controls were included. Serological analysis was performed by routine enzyme-linked immunosorbent assay, and nucleic acid testing for hepatitis viruses was done by polymerase chain reaction (PCR), followed by PCR direct sequencing for viral genotyping. Cytochrome P450 2E1 (CYP2E1) polymorphism was studied by PCR-restriction fragment length polymorphism. Nitrite and volatile nitrosamines in indigenous foods consumed routinely by the Northeast Indian ethnic population were estimated by Griess’s reagent and GC-MS, respectively.RESULTS: Hepatitis A virus (HAV) infection was predominantly prevalent (36.5%) in our cohort, followed by hepatitis B virus (HBV), hepatitis E virus (HEV) andhepatitis C virus. HBV genotype D and HEV genotype 1 were the most dominant. CYP2E1 c1/c2 genotype frequency was comparatively higher in alcoholic (P<0.0001,OR =30.5) and cryptogenic (P=0.014, OR=8.714) patients, and was associated with significantly higher hepatitis risk (P=0.0.007,OR=6.489). Mutant C allele of Cyp2E1 DraⅠ frequency was comparatively higher in HAV (P=0.006), alcoholic (P =0.003) and cryptogenic (P=0.014) cases, and was associated with overall hepatitis risk (P=0.026, OR=5.083). Indigenous foods, Gundruk, Kharoli, betel leaf and nuts were found to have the highest nitrite content. CONCLUSION: Apart from viral factors, CYP2E1 polymorphism might be associated with increased risk of liver diseases in Northeast India. Indigenous foods that contain nitrite and nitrosamine might be an associated risk factor.

<i>Escherichia coli</i>Harbouring Resistance Genes, Virulence Genes and Integron 1 Isolated from Athi River in Kenya

Rivers can act as reservoirs of highly resistant strains and facilitate the dissemination of resistance, virulence and integron 1 genes. A cross-sectional study was carried out where 318 water samples were collected (53 from each site) and from the samples, 318 E. coli isolates were analysed for resistance genes, virulence genes and integron 1 using Polymerase Chain Reaction. 22% of the isolates had blaTEM, 33% had blaCTX-M and 28% had blaCMY. Prevalence of typical Enteropathogenic E. coli strains (carrying both eae and bfp genes) was 5% while the prevalence of atypical Enteropathogenic E. coli (carying only eae) was 1.8%. The prevalence of Enteroaggregative E. coli carrying the aggr genes was 11%. The prevalence of Enterotoxigenic E. coli encoding only lt toxin was 16 (5%) and while those carrying only st toxin was 6.9%. The prevalence of Enteroinvasive E. coli strains encoding as IpaH was 5% while that of strains, adherent invasive E. coli, carrying adherent invasive gene inv was 8.7%. 36% isolates were positive for class 1 integrons which were mostly isolated near the sewage effluent from waste treatment plant. Anthropogenic activities and close proximity to sewage treatment plant were found to play a key role in pollution of water body and accumulation of resistance and virulence genes. These results suggest that waste treatment plant may act as reservoir of resistance, virulence and integron 1 genes and is a potential risk to human and animal health in the region.

硫酸基转移酶SULT1E1、SULT1A1基因多态性与子宫平滑肌瘤易感性的关联研究

目的:探讨硫酸基转移酶SULT1E1、SULT1A1基因多态性对子宫平滑肌瘤易感性的影响。方法:采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)分析法检测子宫平滑肌瘤组和对照组SULT1E1基因rs3736599位点、SULT1A1基因rs9282861位点的多态性情况。结果:①病例组和对照组SULT1E1 rs3736599位点基因型分布差异有统计学意义(P=0.032),携带突变A等位基因(基因型为A/A和A/G)女性发生子宫平滑肌瘤的风险是野生型纯合子G/G女性的3.497倍(P=0.034,OR=3.497,95%CI:1.12～10.91)。②病例组和对照组SULT1A1 rs9282861位点基因型分布差异无统计学意义。结论:硫酸基转移酶SULT1E1基因rs3736599多态性可能与子宫平滑肌瘤易感性相关,携带突变A等位基因可能是子宫平滑肌瘤的危险因素。

乳腺癌组织SULT1E1蛋白表达与临床病理学特征及预后相关性的研究

目的:探讨乳腺癌组织SULT1E1的表达,并分析其与临床病理学特征及预后因素的相关性。方法:采用免疫组织化学二步法检测129例乳腺癌组织和癌旁正常组织SULT1E1的表达情况,应用Kaplan-Meier法行单因素生存分析SULT1E1的表达与临床病理学特征及预后的关系。结果:乳腺癌组织中SULT1E1的阳性表达率(25.6%)明显低于癌旁组织(45.0%),差异有统计学意义,P<0.05;SULT1E1的表达与乳腺癌患者年龄、肿瘤大小、淋巴结转移和病理类型以及是否有远处转移等无明显相关性,P>0.05。Kaplan-Meier生存分析曲线显示,SULT1E1阳性表达患者的术后无复发生存率较阴性表达患者明显增高,χ2=4.943,P<0.05。结论:乳腺癌组织SULT1E1低表达者提示预后不佳,SULT1E1检测有可能成为判断乳腺癌分期和预后的重要分子标志,并成为重要的预后因素。

SULT1E1基因SNP位点在子宫内膜癌中意义的研究

目的 调查SULT1E1基因rs3736599位点在中国北方汉族健康女性人群及子宫内膜癌患者群体中的频率分布数据,分析SULT1E1基因rs3736599位点多态性与子宫内膜癌发病的相关性。方法 采用PCR-RFLP技术筛选不同分型并将其归类,运用全自动DNA测序技术确定单倍型中的突变位点。结果 SULT1E1基因rs3736599位点基因型分布在病例组和对照组差异有统计学意义,χ~2=9.616,P=0.006,用Fisher确切概率法处理得到确切P值（0.006）仍显示有统计学差异;该位点等位基因分布频率在病例组和对照组差异有统计学意义（χ~2=31.736,P=0.000,OR=2.38,95%CI：1.24~4.56）,携带A等位基因患子宫内膜癌的风险是野生型纯合子的2.38倍。结论 硫酸基转移酶SULT1E1基因的rs3736599位点的多态性可能对子宫内膜癌的发病风险有一定影响,并且A等位基因可能对子宫内膜癌的发生和发展产生重影响。

Cloning and analysis of 1-hydroxy-2-methyl-2-(E)-butenyl-4-diphosphate reductase genes HsHDR1 and HsHDR2 in Huperzia serrate

We cloned and analyzed the two genes of the 1-hydroxy-2-methyl-2-(E)-butenyl-4-diphosphate reductase(HDR) gene family from Huperzia serrate.The two transcripts coding HDR,named Hs HDR1 and Hs HDR2,were discovered in the transcriptome dataset of H.serrate and were cloned by reverse transcription-polymerase chain reaction(RT-PCR).The physicochemical properties,protein domains,protein secondary structure,and 3D structure of the putative Hs HDR1 and Hs HDR2 proteins were analyzed.The full-length c DNA of the Hs HDR1 gene contained 1431 bp encoding a putative protein with 476 amino acids,whereas the Hs HDR2 gene contained 1428 bp encoding a putative protein of 475 amino acids.These two proteins contained the conserved domain of 1-hydroxy-2-methyl-2-(E)-butenyl-4-diphosphate reductase(PF02401),but without the transmembrane region and signal peptide.The most abundant expression of Hs HDR1 and Hs HDR2 was detected in H.serrate roots,followed by the stems and leaves.Our results provide a foundation for exploring the function of Hs HDR1 and Hs HDR2 in terpenoid and sterol biosynthesis in Huperziaceae plants.

Exploring the structural and functional effect of pRB by significant nsSNP in the coding region of RB1 gene causing retinoblastoma

In this study,we identified the most deleterious nsSNP in RB1 gene through structural and functional properties of its protein (pRB) and investigated its binding affinity with E2F-2.Out of 956 SNPs,we investigated 12 nsSNPs in coding region in which three of them (SNPids rs3092895,rs3092903 and rs3092905) are commonly found to be damaged by I-Mutant 2.0,SIFT and PolyPhen programs.With this effort,we modeled the mutant pRB proteins based on these deleterious nsSNPs.From a comparison of total energy,stabilizing residues and RMSD of these three mutant proteins with native pRB protein,we identified that the major mutation is from Glutamic acid to Glycine at the residue position of 746 of pRB.Further,we compared the binding efficiency of both native and mutant pRB (E746G) with E2F-2.We found that mutant pRB has less binding affinity with E2F-2 as compared to native type.This is due to sixteen hydrogen bonding and two salt bridges that exist between native type and E2F-2,whereas mutant type makes only thirteen hydrogen bonds and one salt bridge with E2F-2.Based on our investigation,we propose that the SNP with an id rs3092905 could be the most deleterious nsSNP in RB1 gene causing retinoblastoma.

Comparison between homologies of E2/NS1 gene from genotype Ⅲ Chinese isolates of hepatitis C virus and that from reported isolates

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The first E59Q mutation identified in the NEUROD1 gene in a Chinese family with maturity-onset diabetes of the young: an observational study

Objective::In contrast to the most commonly reported forms of maturity-onset diabetes of the young(MODY),including MODY2,MODY3 and MODY5,MODY6 is a relatively rare subtype.To investigate whether NEUROD1 is responsible for MODY in Chinese individuals,we screened its mutations in MODY pedigrees and explored the potential pathogenic mechanisms.Methods::Polymerase chain reaction direct sequencing was performed to screen NEUROD1 mutations in 32 Chinese MODY probands who were negative for the GCK/MODY2,HNF1A/MODY3 and HNF1B/MODY5 genes in this observational study.In addition,we enrolled 201 unrelated,non-diabetic control subjects of Han Chinese descent.The functional significance of newly identified mutations was analyzed using clinical phenotype,pathophysiology and three-dimensional structure studies.This study was approved by the Institutional Review Board of Shanghai Jiao Tong University Affiliated Sixth People’s Hospital,China(approval No.YS-2017-83)on March 3,2017.Results::E59Q(c.175 G>C,p.Glu59Gln),a heterozygous missense mutation in the NEUROD1 gene,was identified in one family with MODY.The Glu59 residue in NeuroD1 is highly conserved across mammalian species.Four diabetic patients carrying the mutation(a proband and her son,brother and sister)were lean,with a body mass index of 20.9(20.3-21.2)kg/m 2.Compared with their unaffected relatives(n=4),E59Q carriers(n=4)had significantly decreased ratios of fasting and 2-hour insulin to plasma glucose(both fasting plasma insulin/fasting plasma glucose and 2-hour postprandial plasma insulin/2-hour postprandial plasma glucose,P<0.005).The proband’s father had an E59Q mutation and normal glucose tolerance,which suggested non-penetrance.The E59Q mutation was not detected in other probands or in the 201 control subjects with normal glucose tolerance.Two salt-bridge bonds of Glu59 were disrupted at the Q59 mutation site.Conclusion::The NEUROD1-E59Q mutation changed the molecular conformation of the N-terminal in NeuroD1,which may decrease binding of the E59Q mutant to the insulin promoter and insulin gene transcription activity,therefore causing the MODY6 subtype with defective insulin secretion.

龙眼参多糖对SAMP8鼠脑组织痴呆相关基因表达的影响

目的观察龙眼参(LYS)多糖对SAMP8(快速老化小白鼠)鼠脑内APP、PS1、PS2、ApoE基因表达的影响。方法选用6mon龄的SAMP8鼠50只,随机分为5组,每组10只:SAMP8对照组、阳性药石杉碱甲对照组、多糖低、中、高剂量组,另选用6monSAMR1(正常老化小白鼠)鼠10只作正常对照组。各组分别灌胃相应药物40d后,采用半定量反转录聚合酶链反应(RT-PCR)来测定SAMP8鼠脑内APP、PS1、PS2、ApoE mRNA含量。结果龙眼参多糖低、中、高剂量能降低脑内APP、PS1、PS2 mRNA含量并呈现一定的量效关系,对ApoE mRNA含量的影响不明显。结论龙眼参多糖能下调SAMP8脑内APP、PS1、PS2基因的表达。

前列腺素E_1抑制血管平滑肌细胞增殖的作用

目的 从细胞周期蛋白和凋亡相关基因探讨前列腺素E1(PGE1)对血管平滑肌细胞 (VSMC)增殖的调控作用。方法 采用培养的新生牛主动脉VSMC ,以胎牛血清及白介素 1(IL 1)分别作为促增殖剂 ,测定不同浓度PGE1对VSMC增殖、细胞内周期蛋白d1mRNA表达、p5 3及Bcl 2基因表达和培养液内NO含量的影响。结果 PGE1浓度依赖性抑制胎牛血清促VSMC增殖作用 ;显著减少细胞周期蛋白d1mRNA含量 ;浓度依赖性诱导IL 1孵育下VSMC产生大量NO ,同时抑制VSMC增殖 ;并促进p5 3基因表达 ,下调bcl 2基因 ,诱导细胞凋亡。结论 PGE1具有抑制VSMC增殖的作用 ,其机制可能与其阻滞VSMC生长有关 ;在炎性因子存在情况下 ,PGE1可诱导VSMC内大量产生NO ,抑制VSMC增殖 ,并加速VSMC凋亡。

HIV-1 gp41基因的分段克隆和表达

目的在大肠杆菌中表达HIV-1gp41N肽和C肽基因。方法用PCR方法从含HIV-1gp160基因的质粒中扩增HIV-1gp41N肽和C肽基因,重组入pGEX-4T-1载体,并亚克隆入pGEM7zf+中测定核苷酸序列,限制性酶切鉴定后进行原核表达。结果成功地扩增到HIV-1gp41N肽和C肽基因,酶切鉴定及测序结果与已知HIV-1亚型的gp41N肽区和C肽区基因序列一致,SDS-PAGE结果显示,表达出与预期分子量大小相同的蛋白。结论N肽和C肽基因的成功表达,为进一步研究其结构和功能奠定了基础。

胃癌组织中MTA1,PTEN,E-cadherin的表达及其相互关系

目的:观察MTA1,PTEN,E-cadherin蛋白在胃癌和正常胃黏膜组织中的表达,探讨其与胃癌浸润、转移和生物学行为的关系．方法:应用免疫组织化学方法检测54例胃癌手术切除标本和15例正常胃黏膜组织中MTA1,PTEN,E-cadherin的表达．各指标之间相关因素的差异性比较采用x2检验,相关性研究采用Spearman相关分析:结果:与正常胃组织相比,MTA1蛋白在胃癌组织中高表达(46．3％vs6．7％,P<0．01),PTEN和E-cadherin蛋白在胃癌组织中表达下调或缺失(51．9％vs 100％,42．6％vs 100％,均P<0．01)．MTA1和PTEN的阳性表达率与肿瘤浸润深度(P=0．003,P=0．001)、病理分期(P=0．004, P=0．008)、淋巴转移(P=0．000,P=0．001)、远隔转移(P=0．004,P=0．006)、临床分期有关(P=0．001,P=0．000);E-cadherin的正常表达率与肿瘤浸润深度(P=0．027)、病理分化程度(P=0．006)、淋巴转移(P=0．044)、临床分期有关(P=0．000)．Spearman相关分析显MTA1与PTEN蛋白、MTA1与E-cadherin蛋白的表达呈负相关(r=-0．518,r=-0．424,均P<0．05)．PTEN蛋白与E-cadherin蛋白的表达呈正相关(r=0．53,P<0．05)．结论:MTA1蛋白水平高表达和PTEN, E-cadherin蛋白水平低表达可能与胃癌浸润和转移有关,且联合检测可以用于判断胃癌的生物学行为．

猪乙脑病毒分离株BSF．ZZ-1和BSF．ZZ-3在BHK-21细胞上的传代培养及E基因序列稳定性分析

为研究猪乙脑病毒(JEV)分离株遗传基因的稳定性,将JEV分离株BSF.ZZ-1和BSF.ZZ-3在BHK-21细胞上进行连续传代培养,并对其E基因的遗传稳定性进行了研究。结果表明,经连续传代60次后病毒E基因趋于稳定,BSF.ZZ-1毒株E蛋白氨基酸位点E21(A→V)、E200(T→A)、E244(G→E)、E279(M→K)和E426(G→D),以及BSF.ZZ-3毒株的E244(G→E)、E255(F→L)、E285(M→L)、E368(L→S)和E497(N→S)传代后发生稳定点突变。与JEV毒力相关的部分位点如E107、E138、E176、E177和E315遗传稳定性较高,经连续传代后均未发生突变,与疫苗株SA14-14-2相应位点完全一致。但是,另外一些位点的遗传稳定性较差,如BSF.ZZ-3的E279(M→K→M)出现反复突变。这些突变是否与JEV的宿主细胞适应性及毒力变化相关有待进一步研究。

几种肿瘤转移基因变化与卵巢癌转移的相关性

目的 研究 MTA1、nm2 3H1 及 E- Cadherin(E- cad)的表达及突变与卵巢癌转移的相关性。方法 应用 RT- PCR、RT- PCR- SSCP和免疫组化技术 ,对正常卵巢、卵巢癌及其配对淋巴结组织进行 MTA1、nm2 3H1m RNA表达和突变及 E- cad蛋白表达的检测。结果 有转移的卵巢癌原发灶 MTA1m RNA高表达率为 10 0 % (7/7) ,无转移为 38.5 % (5 / 13) ,P=0 .0 10 3。有癌转移淋巴结高表达率为 87.5 % (6 / 7) ,而无癌转移为 2 3% (3/ 13) ,P=0 .0 118。有转移卵巢癌原发灶 nm2 3H1 m RNA低表达率为 10 0 % (7/ 7) ,无转移为 30 % (4/ 13) ,P=0 .0 0 43。有癌转移淋巴结低表达率为 10 0 % (7/ 7) ,无癌转移为 38.5 % (5 / 13) ,P=0 .0 10 2。无转移卵巢癌原发灶 E- cad蛋白表达阳性率为 46 .2 % (6 / 13) ,而有转移者 7例均无阳性表达 ,表达率为 0 ,P=0 .0 44。三基因表达相关性分析表明 ,MTA1与 nm2 3H1 、C- cad呈负相关 (r=- 0 .90 3、- 0 .80 2 ) ,nm2 3H1 与 E- cad呈正相关 (r=0 .72 4)。SSCP分析未发现 MTA1和 nm2 3H1 基因突变。结论 MTA1及 nm2 3H1 、E- cad的表达与卵巢癌转移呈正、负相关关系 ,起着正、负调控的重要作用。