胃癌腹膜转移相关基因 MYH-9与胃癌转移及其预后的关系

目的：研究胃癌腹膜转移相关基因MYH-9与胃癌转移及预后的关系。方法50例组织标本取自手术切除的胃癌组织及同一患者的腹膜转移组织标本。组织固定在10％的缓冲甲醛溶液用于病理诊断,冷冻于液氮中备于免疫印迹分析、细胞培养、siRNA转染、细胞粘附实验。结果 MYH-9在所有的鳞状细胞癌组织（100％）和8个邻近正常组织中表达（26．7％,P＝0．000）。癌组织中MYH-9高表达水平与腹膜转移、肿瘤分化程度差和较晚的肿瘤分期显著相关。单变量分析结果显示：肿瘤分期、胃癌病灶是否切除、腹膜转移的存在、MYH9高表达（基于免疫组化染色）与患者总生存率显著相关（P＝0．008、P＝0．001、P＝0．006和P＝0．007）。进一步的多因素回归分析显示,肿瘤分期与MYH-9高表达是与总生存期相关的独立不良预后因素。结论 MYH-9的过度表达可能与较高的癌细胞迁移性相关。     

S100A4协同HIF-1通过WNT/β-catenin通路调控胃癌细胞SGC-7901的迁移和侵袭

目的:探讨S100A4在低氧条件下对胃癌细胞SGC-7901迁移及侵袭的作用及其可能的机制.方法:将化学合成的si-S100A4质粒和阴性对照(si-Ctr1)质粒分别转染胃癌细胞株SGC-7901,根据培养条件的不同分为常氧条件(normal,Nor)+si-S 100A4组、Nor+ si-Ctrl组、低氧条件(hypoxia,Hyp)+si-Ctr1)组、Hyp+si-S 100A4组.应用Western blotting检测低氧条件下胃癌SGC-7901细胞中HIF-1及S100A4蛋白的表达变化,检测低氧条件下胃癌细胞中抑制S100A4的表达对细胞中S100A4、p-catenin及TCF-4表达的影响,Transwell小室法分别检测低氧及S100A4对胃癌SGC-7901细胞迁移及侵袭能力的影响.结果:低氧条件下:(1)胃癌SGC-7901细胞中HIF-1和S100A4表达水平均明显升高(3.12±0.23 vs 1.02±0.05,P＜0.01;2.75±0.32 vs 1.05±0.07,P＜0.01),且两者变化明显相关(r=0.67,P＜0.01);(2)胃癌SGC-7901细胞的侵袭及迁移能力增加[(223.31±35.12) vs (131.29±26.40)、(142.27±26.37)个,P＜0.05].干扰低氧条件中S100A4的表达:(1)明显减少低氧对细胞中Lcatenin及TCF-4的促进作用(均P＜0.01);(2)明显减少低氧对SGC-7901细胞的侵袭及迁移能力的促进作用[(161.37±31.02) vs (88.21±22.42)、(95.36±21.29)个,P＜0.05].结论:S100A4能够促进胃癌细胞SGC-7901的迁移和侵袭,该作用可能是通过S100A4协同HIF-1通过Wnt/β-catenin通路的调控实现的.     

siRNA下调星形细胞上调基因1表达对胃癌SGC-7901细胞增殖和细胞周期的影响

目的 探讨星形细胞上调基因1(AEG-1)表达水平对胃癌细胞增殖和细胞周期的影响,研究其可能的分子机制.方法 以siRNA和AEG-1 siRNA转染胃癌SGC-7901细胞后48 h,将细胞分为未转染组、siRNA对照组和AEG-1 siRNA转染组.应用实时荧光定量PCR和Western blot检测转染后SGC-7901细胞中AEG-1 mRNA和蛋白的表达,应用CCK-8检测细胞增殖能力,应用流式细胞术检测转染前后细胞周期的分布,应用Western blot检测细胞增殖和细胞周期相关蛋白表达的变化.结果 与未转染组和siRNA对照组比较,AEG-1 siRNA转染组胃癌细胞中AEG-1蛋白的表达水平下降(P＜0.05).与未转染组和siRNA对照组比较,AEG-1 siRNA转染组AEG-1 mRNA表达水平下降(P＜0.05).与未转染组和siRNA对照组比较,AEG-1 siRNA转染组转染AEG-1后的24h及其后续的各个时间点,SGC-7901细胞的增殖均明显受到抑制(均P＜0.05).AEG-1 siRNA转染组中G0/G1期细胞数比例[(61.26±1.25)％]显著高于未转染组[(46.17±1.91)％]和siRNA对照组[(46.46±1.96)％],差异均有统计学意义(均P ＜0.05).AEG-1表达水平下降可使cdk2和cyclinD1表达水平下降以及p21表达水平升高.结论 AEG-1表达水平下降抑制胃癌细胞的增殖和改变细胞周期分布,可能与cdk2、cyclin D1和p21蛋白的表达密切相关.     

Bcl-2 siRNA对胃癌细胞凋亡及其紫杉醇敏感性影响研究

目的:研究特异性siRNA对胃癌细胞的抑制作用,以及探讨采用RNA干扰技术下调Bcl-2基因能否增强SGC-7901胃癌细胞对紫杉醇的敏感性。方法:通过脂质体HiperFect将Bcl-2 siRNA转染入胃癌细胞SGC-7901;采用RT-PCR和蛋白印迹法检测Bcl-2 siRNA转染前后胃癌细胞Bcl-2基因表达的变化;用Annexin Ⅴ法及细胞周期分析法检测细胞凋亡;用MTS法观察细胞对药物紫杉醇敏感性的影响。结果:Bcl-2 siRNA组较空白对照组明显抑制Bcl-2 mRNA的表达水平,抑制率为(87.6±5.3)%,P=0.001;Bcl-2 siRNA组较空白对照组明显下调Bcl-2蛋白表达水平,抑制率为(85.7±3.6)%,P=0.003。Bcl-2 siRNA组、紫杉醇组和紫杉醇+Bcl-2 siRNA细胞总凋亡率分别为49.00%、46.10%和66.00%,联合用药组细胞凋亡率最强。Bcl-2siRNA+紫杉醇联合用药对SGC-7901细胞周期分析结果显示,联合用药组凋亡率为48.00%,Bcl-2 siRNA组和紫杉醇组分别为9.03%和21.50%。Bcl-2 siRNA组、阴性对照组和空白对照组的IC50分别(7.25±0.22)、(54.45±0.82)和(68.9±0.91)μg/L,Bcl-2 siRNA转染胃癌细胞SGC-7901对药物紫杉醇更敏感,其IC50值比阴性siRNA转染组降低86.7%,即对紫杉醇敏感性增加7.25倍。结论:靶向Bcl-2 siRNA可明显下调靶基因Bcl-2表达,促进SGC-7901细胞凋亡并能提高细胞对紫杉醇敏感性,为胃癌治疗提供新的策略。     

核因子-κB中介的TNF-α与胃癌细胞侵袭力的相关性

目的 探讨肿瘤坏死闪子(TNF-α)诱导胃癌细胞侵袭力的相关机制.方法 体外培养人胃癌细胞株SGC-7901,采用免疫组化方法检测其在TNF-α不同浓度、时间诱导下的NF-κB活性、uPA蛋白表达强度;采用噻唑蓝(MTT)比色法检测SGC-7901细胞在不同浓度的TNF-α、PDTC(吡咯烷二硫代氨基甲酸盐,NF-κB特异性抑制剂)孵育下的细胞增殖情况;构建侵袭小室,检测不同浓度TNF-α对SGC-7901细胞侵袭力影响,并用PDTC预先处理细胞后.检测其对细胞侵袭力的改变.结果 随着TNF-α浓度的增加和时间延长,SGC-7901细胞NF-κB活性明显增强,90 min为高峰;TNF-α明显上调SGC-7901细胞中的uPA蛋白表达水平;一定范围浓度的TNF-α、PDTC对SGC-7901细胞增殖无明显影响;随着TNF-α浓度增加SGC-7901细胞侵袭数也随之增加,具有明显浓度依赖性(TNF-α5、10、20 μg//L vs 0μg/L,84.33±3.786、108.33±6.110、121.330±4.163 vs 63.330±4.933,F=126.282,P＜0.001),PDTC明显抑制TNF-α诱导的SGC-7901细胞侵袭力(42.330±4.041 vs 63.330±4.933,F=126.282,P＜0.05).结论 TNF-α能够增强胃癌细胞的侵袭力,可能是通过NF-κB信号转导路径,激活uPA等蛋白水解酶而实现的.     

稳定转染Bcl-2 shRNA对胃癌细胞SGC-7901化疗敏感性的影响

目的:探讨稳定转染靶向Bcl-2基因的短发夹RNA(shRNA)对胃癌细胞株SGC-7901化疗敏感性的影响.方法:筛选出稳定转染Bcl-2 shRNA质粒的胃癌SGC-7901细胞株,将其与不同浓度的氟尿嘧啶(5-FU)或顺铂(DDP)作用,未转染的细胞作为对照.RT-PCR法检测稳定转染前后SGC-7901细胞Bcl-2 mRNA的表达水平,MTT法检测5-FU或DDP的IC50,流式细胞仪分析细胞的凋亡率.结果:稳定转染shRNA的胃癌SGC-7901细胞Bcl-2 mRNA的表达明显下降;shRNA联合5-FU的IC50为(14.36±1.63)mg/L,对照组为(35.62±1.95)mg/L,t=2.57,P＜0.05;shRNA联合DDP的半数抑制浓度(IC50)为(2.53±0.46)mg/L,对照组为(6.89±0.52)mg/L,t=2.52,P＜0.05;流式细胞术检测显示,shRNA联合化疗明显提高SGC-7901细胞的凋亡率,t=2.60,P＜0.05.结论:稳定转染Bcl-2 shRNA的胃癌SGC-7901细胞株,其Bcl-2 mRNA的表达能够在较长时间内受到抑制,并提高对化疗药物5-FU及DDP的敏感性.     

干涉Cul1蛋白对胃癌细胞增殖抑制机制的探讨

目的:应用siRNA干涉胃癌细胞中Cul1蛋白表达,观察Cul1蛋白沉默对胃癌细胞增殖的影响,并探计其相关机制.方法:将siRNA转染胃癌细胞BGC-823和SGC-7901,设空白对照组和干涉组,采用蛋白质印迹法检测胃癌细胞BGC-823和SGC-7901中Cul1及PCNA蛋白表达差异.采用CCK8法检测胃癌细胞的增殖活性;流式细胞术(FCM)观察胃癌细胞周期变化.结果:利用siRNA干涉Cul1蛋白表达后,胃癌细胞BGC-823和SGC-7901中Cul1表达水平明显降低,与空白对照组比较有统计学意义,P＜0.01;干涉Cul1蛋白后,其下游相关蛋白-增殖细胞核抗原PCNA表达也明显降低,与空白对照组比较有统计学意义,P＜0.01.CCK8法检测胃癌细胞增殖活性显著降低,与空白对照组比较,差异均具有统计学意义,P＜0.01.流式细胞术观察胃癌细胞周期变化,Cul1蛋白干涉后G1期细胞明显增多,S、G2/M期细胞减少,BGC-823细胞增殖指数(PI)31.68±1.57,干涉Cul1蛋白后PI值为23.74±2.14;SGC-7901 PI值36.04士2.75,干涉Cul1蛋白后PI值为27.29±1.25;两组比较均具有统计学意义,P＜0.05.结论:利用siRNA干涉人胃癌细胞BGC-823、SGC-7901中Cul1蛋白后,胃癌细胞增殖受到明显抑制,其机制可能是通过抑制其下游蛋白PCNA表达.     

胃癌组织Flt-1和PDGFR及bFGFR表达与MVD相关性研究

目的:探讨血管肉皮生长因子受体-1(Flt-1)、血小板衍生生长因子受体(PDGFR)、碱性成纤维生长因子受体(bFGFR)及微血管密度(MVD)的表达及相关性研究.方法:分别选择71例手术切除的胃癌及39例正常胃组织石蜡标本为观察组及对照组,应用免疫组织化学方法检测组织中Flt-1、PDGFR和bFGFR的蛋白表达及MVD.结果:Flt-1、PDGFR和bFGFR在胃癌组织中的阳性率分别为53.5％、49.3％和50.7％,高于对照组(12.8％、10.3％、7.7％),x2值分别为17.514、16.765和20.350,P值均为0.000.且上述受体的表达与胃癌的TNM分期、浸润及淋巴结、远处转移密切相关,P＜0.01或P＜0.05.胃癌组MVD(46.2±15.2)高于对照组(28.6±4.2),t=5.083,P=0.001.MVD与肿瘤的TNM分期、浸润深度、淋巴结和远处转移密切相关,P＜0.01.3种受体在胃癌中的表达存在正相关,P＜0.01.3种受体在胃癌组织中表达均阳性伴有淋巴结转移的发生率为91.7％,高于三者表达均阴性者(68.2％),x2=4.023,P=0.045;向远处转移的发生率分别为58.3％和18.2％,x2=7.769,P=0.005.三者表达均阳性和均阴性的胃癌组织中MVD计数分别为60.5±18.0和40.4±5.1,两组比较差异有统计学意义,t=21.38,P=0.001.结论:3种受体在胃癌组织中表达增高,且与MVD有相关性,它们在胃癌的发生、发展、浸润及转移中可能存在相互诱导及协同作用.     

HIF-1α和CA9在乳腺癌中的表达及其与基底细胞样型乳腺癌的关系

目的 探讨缺氧诱导因子-1α(HIF-1α)和碳酸酐酶9(CA9)在乳腺癌各分子亚型中的表达及其与基底细胞样型乳腺癌的关系.方法 采用免疫组织化学法检测HIF-1α和CA9在5种不同乳腺癌亚型(共803例)中的表达水平并分析其与基底细胞样型乳腺癌临床病理特征及患者生存时间的关系.结果 HIF-1α和CA9在乳腺癌组织中的阳性表达率显著高于癌旁乳腺组织(43.96％∶3.86％,x2=354.858,P＜0.001;19.80％∶4.61％,x2=86.495,P＜0.001).管腔A型、管腔B型、人表皮生长因子受体-2(HER-2)过表达型、基底细胞样型、普通乳腺样型中HIF-1α的阳性表达率分别为31.97％、25.00％、56.06％、77.89％和55.76％,CA9的阳性表达率分别为7.48％、5.56％、60.61％、40.00％和27.88％,差异均具有统计学意义(x2=88.628,P＜0.001;x2=147.128,P＜0.001);HIF-1α和CA9在雌激素受体(ER)阴性的HER-2过表达型、基底细胞样型和普通乳腺样型中的表达明显高于ER阳性的管腔A型和管腔B型(均P＜ 0.005).HIF-1α和CA9的表达与基底细胞样型乳腺癌的淋巴结转移(x2=4.542,P=0.033;x2=7.025,P =0.008)、pTNM分期(x2=5.390,P=0.020x2=10.179,P=0.001)及不良预后有关(x2 =4.353,P=0.037x2=6.056,P=0.014),且二者在基底细胞样型乳腺癌中的表达具有正相关关系(C=0.315,P=0.001).结论 HIF-1α和CA9过表达可能与ER阴性乳腺癌关系更密切,二者可能协同在基底细胞样型乳腺癌的发生、发展中发挥重要作用.基底细胞样型乳腺癌HIF-1α和CA9过表达提示患者预后不良.     

姜黄素对人胃癌细胞SGC-7901的影响

目的 探讨姜黄素对人胃癌细胞SGC-7901的影响.方法 人胃癌细胞SGC-7901接受不同浓度姜黄素处理,然后采用MTT法测定人胃癌细胞SGC-7901的增殖,Boyden chamber侵袭小室测定细胞侵袭能力,划痕实验测定细胞迁移能力.结果 姜黄素能够抑制人胃癌细胞SGC-7901增殖,且作用与药物浓度有关(P＜0.05),浓度越大,抑制能力越强;姜黄素能够抑制人胃癌细胞SGC-7901侵袭、迁移,且作用与药物浓度有关(P＜0.05),浓度越大,抑制能力越强.结论 姜黄素能够抑制人胃癌细胞SGC-7901的增殖、侵袭、迁移,且这种作用具有剂量依赖性.     

Down-regulated miR-9 and miR-433 in human gastric carcinoma

Background

Opioid analgesics are generally used to combat the pain associated with cancerous conditions. These agents not only inhibit respiratory function and cause constipation, but also induce other significant side effects such as addiction and tolerance, all of which further contribute to a reduced quality of life for cancer patients. Thus, in the present study, the effects of electro-acupuncture treatment (EA) on mechanical allodynia were examined in a cancer pain mouse model.

Methods

In order to produce a neuropathic cancer pain model, S-180 sarcoma cells were inoculated around the sciatic nerve of left legs of Balb/c mice. Magnetic Resonance Imaging (MRI) scanning confirmed the mass of S-180 cancer cells embedded around the sciatic nerve. Mechanical allodynia was most consistently induced in the mouse sarcoma cell line S-180 (2 × 10⁶sarcoma cells)-treated group compared to all the other groups studied. EA stimulation (2 Hz) was administered daily to ST36 (Zusanli) of S-180 bearing mice for 30 min for 9 days after S-180 inoculation.

Results

EA treatment significantly prolonged paw withdrawal latency from 5 days after inoculation. It also shortened the cumulative lifting duration from 7 days after inoculation, compared to the tumor control. Also, the overexpression of pain peptide substance P in the dorsal horn of the spinal cord was significantly decreased in the EA-treated group compared to the tumor control on Day 9 post inoculation. Furthermore, EA treatment effectively increased the concentration of β-endorphin in blood and brain samples of the mice to a greater extent than that of the tumor control as well as the normal group. The concentration of β-endorphin for EA treatment group increased by 51.457% in the blood and 12.6% in the brain respectively, compared to the tumor control group.

Conclusion

The findings of this study suggest that a S-180 cancer pain model is useful as a consistent and short time animal model. It also indicated that EA treatment could be used as an alternative therapeutic method for cancer pain due to a consequent decrease in substance P and increase in β-endorphin levels.     

Chromosomal instability in MYH- and APC-mutant adenomatous polyps

The vast majority of colorectal cancers display genetic instability, either in the chromosomal instability (CIN) or microsatellite instability (MIN) forms. Although CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near diploid. Recently, biallelic germ line mutations in the MYH gene were found to be responsible for MYH-associated polyposis (MAP), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant familial adenomatous polyposis (FAP) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser capture microdissection, isothermal genomic DNA amplification, and array comparative genomic hybridization. Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% and 60% of the MAP and FAP polyps showed aneuploid changes, respectively. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19, and 22 and gains affecting chromosomes 7 and 13. The aneuploid changes detected at early stages of MYH-driven tumorigenesis may underlie accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.     

胃癌组织MMP-9基因及蛋白表达与肿瘤临床病理关系研究

目的：研究胃癌患者基质金属蛋白酶-9表达与肿瘤临床病理参数之间相关性。方法：应用酶联免疫吸附（ELISA）方法检测术前外周血清及胃液中MMP-9蛋白水平。结果：胃癌组、对照组血清中金属蛋白酶平均水平分别为406．03±257．18ng／ml、167．35±54．04ng／ml,（P〈0．01）;TNM晚期、淋巴结转移阳性者术前外周血清蛋白含量显著高于TNM早期、淋巴结转移阴性者（P〈0．01）。胃癌组术前胃液中MMP-9蛋白平均水平为77．59±191．97ng／ml,对照组胃液中MMP-9蛋白平均水平为0．81±2．39ng／ml,（P〈0．01）。肿瘤侵犯至浆膜层、TNM晚期、淋巴结转移阳性者蛋白含量显著高于肿瘤未侵犯至浆膜层、TNM早期、淋巴结转移阴性者（P〈0．01）。结论：检测胃癌患者术前胃液中血清中蛋白酶水平能反映肿瘤进展。     

骨桥蛋白与MMP-9在胃癌中的表达及其临床意义

目的:探讨骨桥蛋白(OPN)和MMP-9在胃癌组织的表达及与胃癌转移复发中的关系.方法: 采用免疫组化法检测80例胃癌组织中OPN和MMP-9的表达情况.结果: OPN及MMP-9的在80例胃癌组织中阳性表达率分别为71.25%(57/80)和48.75%(39/80) .OPN的表达与浆膜浸润、术后复发、肝转移、淋巴结转移有关,与临床分期、肿瘤大小及组织学类型无关.MMP-9的表达与临床分期、浆膜浸润、术后复发、肝转移及淋巴结转移有关,与肿瘤大小及组织学类型无关.OPN与MMP-9的表达呈显著正相关(γ =0.288,P=0.010).结论: OPN与MMP-9的表达与胃癌侵袭转移的发生有密切关系,两者均阳性表达时对预测胃癌转移及预后具有指导意义.     

胃癌组织MMP-9基因及蛋白表达与肿瘤临床病理关系研究

目的:研究胃癌患者基质金属蛋白酶-9表达与肿瘤临床病理参数之间相关性。方法:应用酶联免疫吸附(ELISA)方法检测术前外周血清及胃液中MMP-9蛋白水平。结果:胃癌组、对照组血清中金属蛋白酶平均水平分别为406.03±257.18 ng/m l、167.35±54.04 ng/m l,(P<0.01);TNM晚期、淋巴结转移阳性者术前外周血清蛋白含量显著高于TNM早期、淋巴结转移阴性者(P<0.01)。胃癌组术前胃液中MMP-9蛋白平均水平为77.59±191.97ng/m l,对照组胃液中MMP-9蛋白平均水平为0.81±2.39ng/m l,(P<0.01)。肿瘤侵犯至浆膜层、TNM晚期、淋巴结转移阳性者蛋白含量显著高于肿瘤未侵犯至浆膜层、TNM早期、淋巴结转移阴性者(P<0.01)。结论:检测胃癌患者术前胃液中血清中蛋白酶水平能反映肿瘤进展。     

The prognostic significance of gastric juice CA 19-9 and CEA levels in gastric carcinoma patients

AIM: The usefulness of gastric juice CA 19-9 and carcinoembryonic antigen (CEA) levels in the diagnosis of gastric carcinoma is controversial. There is only one study related with their prognostic value. In this study the clinical significance of gastric juice CA 19-9 and CEA levels in patients with gastric carcinoma was investigated. METHODS: Preoperative serum and gastric juice CA 19-9 and CEA concentrations were measured in 139 patients with gastric carcinoma, 54 patients with benign gastroduodenal disease and as the 'healthy' control group 46 patients with inguinal hernia and with no other pathology. RESULTS: In all groups the mean gastric juice levels of CA 19-9 and CEA were significantly higher than the serum levels. The gastric juice CA 19-9 levels were not different between groups. Gastric juice CEA levels of the gastric carcinoma group were significantly higher than those of the benign gastroduodenal disease group (P=0.007) and had a tendency to increase when compared to those of the control group (P=0.064) whereas there was no significant difference between the benign gastroduodenal disease and the control group. The cut-off values of gastric juice CA 19-9 and CEA were 440U/ml and 320ng/ml and the positivity ratios of these markers in gastric carcinoma patients were 16.5 and 27.3%, respectively. There was no significant relationship between the histopathological features and the gastric juice CA 19-9 or CEA positivities. Neither univariate analysis nor the multivariate Cox proportional hazards model analysis showed prognostic value for gastric juice CA 19-9 and CEA positivities. CONCLUSIONS: The gastric juice CA 19-9 and CEA levels have no diagnostic and prognostic significance in gastric carcinoma patients.     

CD147和MMP-9在胃癌组织中的表达及其与预后的关系

目的:探讨细胞外基质金属蛋白酶诱导因子(extracellular matrix metalloproteinase inducer,CD147)和基质金属蛋白酶-9(matrix metalloproteinases-9,MMP-9)在胃癌中的表达,两者的关系及其与胃癌浸润、转移和预后的关系。方法:应用免疫组化SP法检测63例胃癌组织及40例癌旁正常组织CD147、MMP-9蛋白的表达,并与临床病理参数和预后进行对比。结果:胃癌组织中CD147和MMP-9的阳性表达率分别为77.8%和81.0%,均明显高于癌旁正常组织中的表达率（25.0%和25.0%）（P均＜0.05）。CD147和MMP-9的表达都与肿瘤浸润深度、TNM分期、淋巴结转移及Ki-67增殖指数相关（P＜0.05）。CD147和MMP-9的表达呈正相关（r=0.907,P=0.000）。单因素生存分析显示CD147和MMP-9表达阳性的胃癌患者生存率低于表达阴性组。结论:CD147和MMP-9与胃癌侵袭和转移有关,CD147与MMP-9的产生有密切的关系,两者可作为胃癌判断临床预后的参考指标。     

MMP-9、Cath-D阳性与胃癌生物学行为相关性

目的:探讨MMP-9和Cath-D阳性与胃癌生物学行为的关系。方法:采用免疫组化S-P法,检测MMP-9和Cath-D在128例原发性胃癌的阳性率。结果:128例胃癌组织中MMP-9和Cath-D阳性表达与胃癌生长方式、浸润深度、TNM分期、淋巴结转移密切相关(P<0.05);弥漫型胃癌MMP-9阳性率明显高于肠型胃癌(P<0.01);MMP-9和Cath-D阳性的胃癌患者五年生存率较阴性者低(P<0.05);两者在胃癌中阳性呈正相关,MMP-9(-)/Cath-D(-)组发生淋巴结转移和浆膜浸润的比率均明显低于MMP-9( )/Cath-D( )组、MMP-9( )/cath-D(-)组和MMP-9(-)/Cath-D( )组(P<0.05)。结论:MMP-9和(Sath-D与胃癌的生长、浸润、转移及预后均有密切关系,同时进行MMP-9和Cath-D免疫组化检测对于评估胃癌的预后有意义。     

KiSS-1和MMP-9在胃癌及其癌前病变中的表达和临床病理意义

目的:检测KiSS-1与MMP-9在胃癌中的表达,分析两者与胃癌临床病理因素以及患者临床预后之间的关系,探讨KiSS-1和MMP-9在胃癌发生发展中的作用.方法:将162例胃癌及配对正常组织构建于组织芯片上,采用免疫组化两步法检测KiSS-1和MMP-9的表达.结果:胃癌组织中KiSS-1的阳性表达率(67.90％,110/162)显著低于正常黏膜(83.95％,136/162)、慢性萎缩性胃炎(90.48％,38/42)和肠上皮化生(83.87％,78/93)中的阳性率,P＜0.05.胃癌组织(78.40％,127/162)、慢性萎缩性胃炎(52.38％,22/42)和肠上皮化生(68.82％,64/93)中MMP-9的阳性表达率显著高于正常黏膜(31.48％,51/162).MMP-9在肠型胃癌(90.48％,38/42)中的阳性表达率显著高于弥漫型胃癌(74.11％,83/112) (P ＜0.05).MMP-9表达强阳性组和其他组相比[(15.2±4.8)个月vs (35.0±2.9)个月],平均生存时间较短,差异有统计学意义(P =0.032).结论:与正常胃黏膜相比,胃癌组织中存在着KiSS-1表达下调和MMP-9表达的上调,可能在胃癌发生发展过程中发挥着重要作用.此外,MMP-9的强阳性表达与不良预后有关.