单唾液酸神经节苷脂3对人肺腺癌细胞增殖凋亡及血管内皮生长因子表达的影响

目的 研究外源性单唾液酸神经节苷脂3(GM3)对人肺腺癌细胞增殖、凋亡和血管内皮生长因子(VEGF)表达的影响,探讨GM3的抗肿瘤作用.方法 以不同浓度外源性GM3干预人肺腺癌A549细胞48 h,采用四甲基偶氮唑蓝(MTT)法检测细胞增殖变化,Annexin V-FITC/PI双染流式细胞学技术检测细胞凋亡变化,逆转录聚合酶链反应(RT-PCR)检测细胞VEGF mRNA的表达水平,激光共聚焦显微镜观察细胞VEGF蛋白的表达变化.结果 2.5、10、40、160和640 μmol/L GM3干预A549细胞48 h,增殖抑制率分别为4.1%、8.9%、29.9%、34.2%和52.6%,GM3作用于A549细胞48 h的半数抑制浓度(IC50)为412 μmol/L.与对照组相比,当GM3＞10 μmol/L时,对细胞增殖抑制作用明显(P＜0.05),且具有浓度依赖性.10、40和160μmol/L GM3干预A549细胞48 h,A549细胞的凋亡率分别为(1.3±0.6)%、(4.8±0.4)%、(14.2±1.0)%.与对照组相比,当GM3＞40 μmol/L时,其促进细胞凋亡作用明显(P＜0.05).与对照组相比,经浓度＞40 μmol/L的GM3干预后,A549细胞的VEGF mRNA表达水平显著下降(P＜0.05).随着GM3浓度增高,A549细胞的VEGF荧光强度明显减弱.结论 GM3能呈浓度依赖性抑制人肺腺癌细胞株A549增殖,促进A549细胞凋亡,下调A549细胞VEGF mRNA和蛋白水平的表达,提示GM3可能通过调节肿瘤细胞凋亡和肿瘤血管生成而发挥双重抗肿瘤作用.

Abstract：

Objective To determine the effect of exogenous GM3 on proliferation, apoptosis and VEGF expression in human lung adenocarcinoma cell line A549 cells.Methods A549 cells were treated with GM3 at different concentrations for 48 hours.MTT assay was used to detect the cell proliferation and flow cytometry was applied to analyze cell apoptosis.RT-PCR was used to detect the expression level of VEGF mRNA and confocal laser scanning microscopy was applied to observe the localization and fluorescence intensity of VEGF.Results Comparing with the control, being treated with higher than 10μmol/L GM3 significantly inhibited A549 cell proliferation ( P ＜ 0.05 ), and the suppressive effect could be enhanced following increasing doses.The IC50 was 412 μ mol/L.Comparing with the control, being treated with higher than 40 μmol/L GM3 significantly promoted the apoptotic rate of A549 cells ( P ＜ 0.05 ).Comparing with the control, being treated with higher than 40 μ mol/L GM3 significantly decreased the VEGF mRNA level of A549 cells (P＜0.05), and the fluorescence intensity of VEGF distinctly weakened.Conclusions Exogenous ganglioside GM3 can inhibit the proliferation, promote apoptosis, and down-regulate the VEGF expression level in A549 cells.This may be considered as two mechanisms of GM3 for its anti-tumor effect by modulating cell apoptosis and angiogenesis.     

As2O3和全反式维甲酸对人宫颈癌HeLa细胞生长的影响

目的 探讨As2O3和全反式维甲酸(ATRA)对人宫颈癌HeLa细胞体外生长的影响及其机制.方法 采用不同浓度As2O3和ATRA分别作用于人官颈癌HeLa细胞,观察细胞形态;采用四甲基偶氮唑蓝(MTT)比色法检测细胞生长情况;半定量逆转录聚合酶链反应(RT-PCR)和Westernblot法检测细胞中N-myc下游调节基因1(NDRG1)mRNA和蛋白的表达.结果 As2O3和ATRA能够抑制宫颈癌HeLa细胞生长,12.5 μmol/L As2O3处理HeLa细胞48 h的抑制率为(36.5±1.2)%,明显高于同时间低浓度组;1 × 10-5mol/LATRA处理HeLa细胞48 h的抑制率为(23.5±3.1)%,明显高于同时间低浓度组,并且同浓度的药物处理72 h的抑制率高于处理48 h的抑制率,呈浓度和时间依赖性(P<0.05).As2O3和ATRA能够从分子水平和蛋白水平上调宫颈癌HeLa细胞中NDRG1基因的表达,12.5 μmol/L As2O3和5×10-6mol/L ATRA处理HeLa细胞后,NDRG1 mRNA表达量分别为0.942±0.169和0.894±0.138,明显高于低浓度组的表达量;12.5 μmol/LAs2O3和5×10-6 mol/LATRA处理HeLa细胞后,NDRG1蛋白表达量分别为1.220±0.202和1.233±0.103,明显高于低浓度组的蛋白表达量.结论 As2O3能够抑制宫颈癌HeLa细胞生长,其抑制作用与NDRG1基因的表达上调相关.

Abstract：

Objective To study the effect of arsenic trioxide (As2O3 ) and all-trans retinoic acid ( ATRA ) on human cervical carcinoma HeLa cell line.Methods HeLa cells were treated with As2O3 and ATRA.The cell proliferation was evaluated by MTT assay.The expressions of NDRG-1 protein and mRNA were determined by Western blot and RT-PCR analysis.Results MTT assay showed that As2O3 and ATRA inhibited the growth of human cervical carcinoma HeLa cells in vitro in a dose- and time-dependent manner.Western blot and RT-PCR techniques showed that As2O3 and ATRA down-regulated the expressions of NDRG-1 protein and mRNA (P < 0.05 ) .Conclusion As2O3 and ATRA can significantly inhibit the growth and proliferation of HeLa cells.The reason of these changes may be related with the down-regulation of expression of NDRG-1.     

槲皮素对宫颈癌HeLa细胞增殖影响机制探讨

目的：研究植物化学药物槲皮素对宫颈癌细胞的生长抑制作用和凋亡诱导效应,并探讨槲皮素对抗宫颈癌的可能作用机制。方法：采用浓度为10、20、40、80和160μmol/L槲皮素处理HeLa细胞,四唑盐比色法（MTT法）检测不同浓度在作用24、48和72h对HeLa细胞增殖的影响;流式细胞仪分析槲皮素对HeLa细胞凋亡的影响;逆转录-多聚酶链反应（RT-PCR）和蛋白质印迹法检测细胞内的MK和Caspase-3基因mRNA和蛋白表达水平。结果：槲皮素能抑制HeLa细胞增殖,且在一定浓度范围内呈时间浓度依赖性,P〈0.05;使用浓度为10μmol/L的槲皮素处理HeLa细胞48h凋亡率为（2.18±0.04）%,20μmol/L为（3.75±0.11）%,40μmol/L为（6.04±0.07）%,80μmol/L为（9.65±0.04）%,160μmol/L为（21.41±1.81）%,与空白对组的（1.64±0.12）%比较差异有统计学意义,F=300.80,P〈0.01;随槲皮素浓度的增高HeLa细胞中MK mRNA和蛋白表达依次下降,其中80和160μmol/L组下降较明显,而Caspase-3的mRNA和蛋白表达随药物浓度增高表达增强,P〈0.01。MK与Caspase-3的蛋白表达呈负相关,r=-0.922,P〈0.01;MK与Caspase-3的mRNA表达呈负相关,r=-0.955,P〈0.01。结论：槲皮素可显著抑制HeLa细胞增殖并诱导其凋亡,其机制可能通过下调MK、上调Caspase-3的表达水平而发挥抗宫颈癌作用。     

Toll样受体8在人宫颈癌细胞株HeLa中的表达及其激动剂对HeLa细胞增殖和凋亡的影响

目的 观察Toll样受体8(TLR8)在人官颈癌细胞株HeLa中的表达,探讨TLR8激动剂CL075对HeLa细胞增殖和凋亡的影响。方法 采用实时荧光定量聚合酶链反应(PCR)法,检测13种肿瘤细胞系中TLR8 mRNA和经CL075作用后HeLa细胞中环氧化酶2(COX-2)、Bcl-2和血管内皮生长因子(VEGF) mRNA的表达水平;采用免疫荧光技术对HeLa细胞中TLR8蛋白的表达进行定位观察;采用流式细胞术检测不同浓度CL075作用下HeLa细胞的细胞周期和凋亡的变化;采用四甲基偶氮唑蓝(MTT)法检测HeLa细胞的增殖状态。结果 与其他肿瘤细胞株相比,HeLa细胞中TLR8mRNA的表达水平最高,达703.7±20.6。TLR8蛋白主要定位于HeLa细胞的胞浆中。0.1、0.5和1.0 μg/ml的CL075分别作用于HeLa细胞48 h后,G2/M+S期细胞所占的比例逐渐增高,其中1.0μg/ml CL075作用组G2/M+S期细胞所占的比例最高,达(57.67±1.73)％,明显高于空白对照组[(39.02±2.33)％,P＜0.01]。经不同浓度的CL075处理后,HeLa细胞的凋亡水平与空白对照组相比,无明显改变(P＞0.05);但经顺铂处理后,凋亡细胞明显增多(P＜0.01)。MTT法检测结果显示,与空白对照组比较,CL075作用于HeLa细胞48和72 h后,HeLa细胞的增殖能力明显增强(P＜0.01)。CI075作用于官颈癌HeLa细胞24和48 h后,COX-2、Bcl-2和VEGF mRNA的表达水平明显升高(P＜0.05)。结论宫颈癌HeLa细胞中TLR8的表达水平及其与配体相互作用的信号,可能是肿瘤发生和发展的重要因素之一。TLR8可能是宫颈癌治疗的一个潜在靶点。     

自噬在熊果酸抑制人宫颈癌HeLa细胞增殖中的作用

[目的]分析自噬在熊果酸抑制人宫颈癌HeLa细胞增殖中的作用.[方法]体外培养人宫颈癌HeLa细胞,不同浓度(5、10、20μmol/L)的熊果酸处理48h后,采用MTT法检测HeLa细胞增殖抑制率的变化;透射电镜观察细胞自噬超微结构的改变;Western blotting检测自噬相关蛋白p62及Beclin-1的表达情况;微管相关蛋白1轻链3A/B (microtubule-associated protein 1 light chain 3 A/B,LC3A/B)免疫荧光检测熊果酸对HeLa细胞自噬水平的影响;检测自噬抑制剂3-甲基腺嘌呤(3-methyladenine,3-MA)抑制自噬前后对熊果酸增殖抑制作用的影响.[结果]不同浓度(5、10、20 μmol/L)的熊果酸处理组对HeLa细胞的抑制率分别为20.1％±1.3％、35.6％±2.6％和49.0％±1.0％,熊果酸可抑制HeLa细胞增殖并呈剂量依赖性(=446.177,P＜0.001);熊果酸能诱导HeLa细胞发生自噬:透射电镜观察发现经熊果酸处理后HeLa细胞中自噬囊泡明显增加;Western blotting分析表明熊果酸可呈剂量依赖性增加Beclin-1的表达,降低p62的表达;免疫荧光检测显示熊果酸处理后,HeLa细胞的荧光强度与对照组相比明显增强;3-MA与熊果酸联合作用于HeLa细胞时可抑制细胞增殖.[结论]熊果酸抑制HeLa细胞增殖,并诱导其发生自噬,自噬抑制剂3-MA能够增强熊果酸对HeLa细胞的增殖抑制作用.     

2,3-吲哚醌诱导成神经细胞瘤SH-SY5Y细胞凋亡过程中部分凋亡调控基因的变化

目的:研究2 ,3-吲哚醌(2, 3-dioxoindoline, isatin,ISA)诱导人成神经细胞瘤SH-SY5Y细胞凋亡的分子机制.方法:体外培养人成神经细胞瘤SH-SY5Y细胞,将SH-SY5Y细胞随机分为对照组和ISA不同浓度(100、200和400 μmol/L )处理组,采用Hoechst 33258荧光染色、DNA ladder分析细胞凋亡,RT-PCR检测不同浓度ISA处理后基因VEGF、bcl-2、 bax、survivin及p53在mRNA水平上表达的变化,FCM法检测caspase-3蛋白表达的变化.结果:不同浓度的ISA(0、100、200和400 μmol/L)作用SH-SY5Y细胞48 h后,在荧光显微镜下观察到400 μmol/L ISA组细胞出现典型的凋亡形态学改变:细胞核染色质聚集、碎裂,细胞质浓缩;琼脂糖凝胶电泳显示400 μmol/L ISA处理组细胞出现明显的梯状条带.RT-PCR结果显示:随着ISA作用浓度的增加,bcl-2、VEGF和survivin mRNA的表达均逐渐减少(P<0.05),bax mRNA表达水平未见明显变化(P>0.05) ;而随着ISA浓度的增加, p53 mRNA表达水平逐渐增加(P<0.05),并呈浓度依赖关系.FCM结果显示,随着ISA作用浓度的增加,活化的caspase-3蛋白表达率分别为18.38%、26.93%和35.66%,明显高于对照组的11.23%(P<0.05).结论:ISA能明显诱导SH-SY5Y细胞凋亡,其机制可能与ISA促进p53 mRNA转录、抑制bcl-2和survivin mRNA转录以及使细胞内活化的caspase-3蛋白水平增加有关.另外,ISA能抑制VEGF mRNA转录,对抑制肿瘤生长及转移有重要意义.     

索拉非尼对宫颈癌细胞的增殖抑制作用及对PCNA、Survivin表达的影响

目的 探讨索拉非尼对宫颈癌细胞株增殖和凋亡的影响。方法体外培养宫颈癌HeLa、SiHa细胞株,实验分为空白对照组、阴性对照组（DMSO）和索拉非尼（0、25、5、10、20 μmol／L）处理组。光学显微镜观察各组细胞形态学改变;Hoechst荧光染色观察凋亡细胞核的形态学变化;采用MTS法检测索拉非尼对HeLa和SiHa细胞的增殖抑制作用;免疫细胞化学法检测索拉非尼（10 μmol／L）处理HeLa、SiHa细胞48 h后Survivin蛋白的表达;Western blotting检测索拉非尼对宫颈癌HeLa、SiHa细胞PCNA、Survivin蛋白表达的影响。结果不同浓度索拉非尼作用48 h后,HeLa、SiHa细胞出现了凋亡形态学改变;Hoechst染色显示,HeLa、SiHa细胞的胞核变小、固缩,荧光明显增强。MTS检测显示,索拉非尼可抑制宫颈癌HeLa、SiHa细胞增殖,并呈浓度依赖性（P＜0.05）。免疫细胞化学法检测显示,阴性对照组Survivin在HeLa和SiHa细胞中的平均光密度值分别为0.19±0.05和0.17±0.07,与索拉非尼处理组的0.13±0.01和0.13±0.03比较,差异均有统计学意义（P＜0.05）。Western blotting检测显示,索拉非尼在蛋白水平上能够降低PCNA、Survivin表达,且这种下调作用具有浓度依赖性。结论索拉非尼能诱导HeLa、SiHa细胞凋亡,抑制其增殖且呈浓度依赖性,其机制可能与下调癌基因 PCNA、Survivin表达有关。     

硫化砷对人宫颈癌HeLa细胞增殖和凋亡及COX-2表达的作用

目的:体外研究中药雄黄的主要成分硫化砷(As4S4)对子宫颈癌HeLa细胞的增殖抑制和诱导凋亡的作用及与环氧合酶-2(cyclooxygenase-2, COX-2)表达的关系.方法:以不同浓度的As4S4 (7.5～60 mg/L),分12～60 h 5个时间点处理HeLa细胞,四甲基偶氮唑蓝(MTT)法测定细胞增殖抑制率;DNA梯状电泳检测凋亡的发生; Western blot检测COX-2蛋白的表达;放射免疫法检测细胞前列腺素E2(prostaglandin E2, PGE2)释放水平.结果: As4S4可抑制HeLa细胞增殖,作用呈明显的时效和量效关系,P＜0.01;As4S4可诱导HeLa细胞凋亡,DNA电泳呈梯状条带;As4S4可明显抑制COX-2的表达,P＜0.01,并呈浓度依赖性;As4S4明显抑制HeLa细胞PGE2释放水平,其值分别为(70.56±2.03)、(48.58±2.28)、(29.25±1.57)和(18.02±1.04) μg/L,与对照组(83.15±1.01) μg/L比较差异有统计学意义,P＜0.01.结论: As4S4 体外对HeLa细胞具有增殖抑制和促进凋亡作用,其机制可能与抑制COX-2蛋白表达有关.     

白花丹素对骨肉瘤MG-63细胞迁移的影响及其作用机制

目的 观察白花丹素对骨肉瘤细胞迁移的抑制作用并初步探讨其可能的机制.方法 以2.5 μmol/L、5μmol/L和10 μmol/L浓度白花丹素分别作用于骨肉瘤MG-63细胞,以含0.1％ DMSO完全培养基为对照组.作用24 h后,Transwell法观察骨肉瘤MG-63细胞迁移能力,Real-time PCR检测骨肉瘤MG-63细胞中Ezrin基因mRNA表达情况,Westem blot检测Ezrin蛋白和p-Ezrin的表达情况.结果 Transwell结果显示,作用24h后,各实验组下层小室细胞数明显减少,2.5 μmol/L组、5μmol/L组和10 μmol/L组的细胞迁移率分别为(69.9±4.5)％、(39.3±3.5)％和(26.2±4.1)％,呈浓度依赖性(P＜0.05);Real-time PCR结果显示,骨肉瘤MG-63细胞中Ezrin mRNA表达水平明显下降,呈浓度依赖性(P＜0.05).Western blot结果显示,Ezrin蛋白和p-Ezrin的表达量明显降低,呈浓度依赖性(P＜0.05).结论 白花丹素能够抑制骨肉瘤MG-63细胞迁移,其作用机制可能与抑制骨肉瘤MG-63细胞中Ezrin的表达及活化有关.     

人肝癌细胞感染蓝舌病毒HbC_3株超微结构的动态观察

目的探讨蓝舌病毒靶向抗肿瘤的细胞生物学机制。方法利用透射电镜观察蓝舌病毒HbC3株感染人肝癌细胞Hep-3B的形态发生学以及该病毒引起的细胞的病理改变。结果BTV-HbC3以受体介导的胞饮作用穿入细胞,溶酶体水解病毒外衣壳,使之成为亚病毒粒子,胞浆内有病毒包涵体及未装配成熟的亚病毒颗粒。随后亚病毒颗粒装配上外层蛋白结构,形成成熟的病毒粒子。病毒感染细胞12~18h时,细胞以挤出的方式释放病毒并达到高峰。18~48h时,病毒进入超感染期,大量细胞发生病变,出现细胞凋亡和溶解。结论一旦蓝舌病毒感染Hep-3B肿瘤细胞即可在细胞内增殖并诱导该肿瘤细胞进入凋亡,死亡的肿瘤细胞释放出的病毒粒子并再次感染其他肿瘤细胞,直至将全部肿瘤细胞杀灭,其溶瘤方式为链式反应。     

Construction of a recombinant eukaryotic expression vector containing PHD3 gene and its expression in HepG2 cells

ABSTRACT: Prolyl hydroxylase domain 3 (PHD3) is a hypoxia inducible factor-alpha (HIFalpha) regulator; it degrades HIFalpha in the presence of oxygen. Recently, there have been an increasing number of studies about the role of PHD3 in proliferation and apoptosis of cancer cells. However, most of the evidence for the role of PHD3 is observational, and little is known of the molecular mechanism. In our current study, we constructed a recombinant eukaryotic expression vector containing the PHD3 gene and detected its biological activity in human hepatoma cell line (HepG2 cells). We successfully constructed a recombinant pcDNA 3.1(+)-PHD3 plasmid; the results showed that PHD3 overexpression could inhibit the proliferation of HepG2 cells and induce apoptosis by activating caspase-3 activity. Our study has provided preliminary materials and data for further investigation of the effect of PHD3 on HepG2 cells.     

联合检测AFP-L3％、GP73、GPC3在AFP低值原发性肝癌诊断中的价值

目的:本研究探讨血清甲胎蛋白异质体3百分含量(AFP-L3％)、高尔基蛋白73(GP73)、磷脂酰肌醇蛋白聚糖3(GPC3)联合检测在AFP低值原发性肝癌(primary hepatic carcinoma,PHC)诊断中的临床价值.方法:选取58例AFP低值原发性肝细胞癌患者(PHC组)、62例良性肝病患者(良性肝病组)和55例体检健康者纳入本研究.采用微量离心柱法分离AFP-L3,电化学发光法检测AFP与AFP-L3,计算AFP-L3％.依据试剂盒推荐以AFP-L3％≥10％作为阳性界值.采用酶联免疫吸附法检测GP73、GPC3血清浓度,其诊断PHC的cut-off值由受试者工作特征曲线(recover operation characteristic,ROC)确定.结果:PHC组AFP-L3％ (16.58％±5.12％)明显高于良性肝病组(9.16％±3.86％)和健康对照组(5.11％ ±2.03％,P＜0.001);PHC组GP73浓度(167.83±69.56) ng/ml明显高于良性肝病组(59.43±28.37) ng/ml和健康对照组(10.39±4.22) ng/ml,P＜0.001;PHC组GPC3浓度(116.52±48.21) μg/L明显高于良性肝病组(28.43±11.25)μg/L和健康对照组(3.25±1.46) μg/L,P＜0.001.以AFP-L3％≥10％作为阳性界值诊断PHC,诊断灵敏度为82.76％,特异度为82.05％,诊断正确率为82.28％;依据ROC曲线,GP73诊断PHC的cut-off值为81.86 ng/ml,诊断灵敏度为77.59％,特异度为82.91％,诊断正确率为81.14％;依据ROC曲线,GPC3诊断PHC的cut-off浓度为35.43μg/L,诊断灵敏度为70.69％,特异度为77.78％,诊断正确率为75.43％;联合检测AFP-L3％、GP73、GPC3水平诊断PHC的灵敏度为87.93％,特异度为84.62％,诊断正确率为85.71％.结论:肿瘤标志物AFP-L3％、GP73、GPC3可作为早期诊断和鉴别诊断PHC的良好指标,联合检测可显著提高诊断正确率.     

维生素D3与结直肠癌相关性的研究进展

越来越多的研究证据已经表明,血清中低水平的维生素D₃（VD₃）与较高的结直肠癌（CRC）风险相关。目前大多数的观察性研究支持血清中25-(OH)-VD₃水平与CRC风险呈负相关性。然而,口服VD3或饮食中补充VD₃可否改善CRC患者的总生存期,目前还存在争议。本文将对近年来VD₃与CRC相关性的研究作一综述,以期有更多前瞻性的基础研究、临床研究和人群观察性研究对VD3是否对CRC的预防和治疗有价值做出澄清。     

A Meta-analysis of Ginsenoside Rg3 for Non-small Cell Lung Cancer

OBJECTIVE Ginsenoside Rg3 (Rg3) has shown anti-tumor effects on various tumor cells. It has been widely used in China for non-small cell lung cancer (NSCLC). However, there are only a few clinical trials to study the effectiveness of Rg3 on NSCLC, and almost them are smallsamples,so we performed a meta-analysis on the results of the studies we collected in order to investigate the effectiveness of Rg3 on NSCLC.METHODS A meta-analysis was conducted in all the selected randomized controlled trials evaluating the effectiveness of Rg3 on NSCLC patients. All on-line databases regarding Rg3 from 1950 to 2011 were searched. Supplemental hand searching of the references of retrieved articles was performed.RESULTS Six trials met the inclusion criteria. Four of them compared chemotherapy plus Rg3 with chemotherapy alone, and the other 2 compared chemotherapy plus Rg3 with chemotherapy plus placebo. These trials are homogeneous. Two of the trials report overall survival, but the data are not suitable for a meta-analysis.After meta-analysis was conducted in the included studies comparing the effects of chemotherapy plus Rg3 with that of chemotherapy alone or chemotherapy plus placebo, it was suggested that chemotherapy plus Rg3 increased the response rate [odds ratio: 2.64 (95% CI: 1.70-4.11), fixed effects model] and disease control rate [odds ratio: 3.34 (95% CI: 1.92-5.81); fixed effects model] of the patients at stage II-IV, especially for the patients at stage III-IV.CONCLUSION Meta-analysis of the available evidence suggests that Rg3 plus chemotherapy improves the response rate of NSCLC patients, and well-designed RCTs with large sample size are needed.     

Diagnostic and prognostic value of MATN3 expression in gastric carcinoma: TCGA database mining

BackgroundsGlobally, the high morbidity and mortality of gastric carcinoma (GC) have been one of the great challenges facing humanity. However, the early diagnosis of GC is still unknown. Matrilin-3 (MATN3) is a member of the extracellular matrix (ECM) protein family. Previous studies have reported a correlation between the expression of MATN3 and bone disease. However, the role of MATN3 in GC has not been reported in depth, which can have a possible far-reaching implication for GC.MethodsWe explored the diagnostic and prognostic value and pathway enrichment of MATN3 expression in GC. Limma package conducted by R was used to analysis the difference expression data of MATN3 from The Cancer Genome Atlas (TCGA). The receiver operating characteristic (ROC) curve analysis was used to estimate the diagnostic value of MATN3 expression. univariate and multivariate analysis were used to assess the prognostic value of MATN3, and gene set enrichment analysis (GSEA) to identify the enriched signaling pathways.ResultsMATN3 was found to be significantly higher in GC tissue samples. GC patients with high MATN3 expression had poor prognosis. Then, GSEA showed that the gene sets were correlated with signaling pathways including ECM receptor interaction, hypertrophic cardiomyopathy (HCM), and glycosaminoglycan biosynthesis chondroitin sulfate, among others.ConclusionsThe study suggests that MATN3 can serve as a potential diagnostic and prognostic biomarker for GC.     

Galectin-3 leads to attenuation of apoptosis through Bax heterodimerization in human thyroid carcinoma cells

Cancer cells survive escaping normal apoptosis and the blocks in apoptosis that keep cancer cells alive are promising candidates for targeted therapy. Galectin-3 (Gal-3) is, a member of the lectin family, which is involved in cell growth, adhesion, proliferation and apoptosis. It remains elusive to understand the role of Gal-3 on apoptosis in thyroid carcinoma cells. Here, we report that Gal-3 heterodimerizes Bax, mediated by the carbohydrate recognition domain (CRD) of Gal-3, leading to anti-apoptotic characteristic. Gal-3/Bax interaction was suppressed by an antagonist of Gal-3, in which in turn cells became sensitive to apoptosis. The data presented here highlight that Gal-3 is involved in the anti-apoptosis of thyroid carcinoma cells. Thus, it suggests that targeting Gal-3 may lead to an improved therapeutic modality for thyroid cancer.     

主动呼吸控制技术(ABC)在肺癌放射治疗中的应用

目的：使用主动呼吸控制技术（aetive brething control,ABC）治疗非小细胞肺癌患者，评价呼吸运动时肺部肿瘤动度的影响及ABC技术的优势和可行性，并评价近期疗效和急性放射反应。方法：选择9例使用ABC技术联合三维造型放疗技术治疗的非小细胞系癌患者进行分析。CT定位扫描时分别采集ABC和自由呼吸（free breath.FB）状态下的图像，评价呼吸运动对肺部肿瘤动度和PTV边界的影响唾弃；并比较两种计划的DVH，放疗剂量为54-60Gy/18-20次。3Gy/次，1次/天，5天/周，定期随访，评价近期疗效及急性放射反应。结果：应用ABC技术后，隔肌的平均位移从FB时的43.5mm（20.0-32.0mm）降低为3.6mm（0.5-72.mm）,胸壁的侧方位移从FB时的3.2mm（2.8-4.0mm）降低为1.2mm（0.5-1.6mm）.PTV边界可以从FB时的1.5mm减少为0.75cm;肺的V20从21.8%降低为15.0%,减少了30.6%.中位随访6个月时,9例患者中有6例CR,3例PR.急性放射副反应都很轻微,仅为I-II.结论：在肺癌的精确放射治疗中,呼吸动度的影响不可忽视.而ABC系统可以有效的降低呼吸运动时治疗的影响,提高放疗的精确性,减少副反应.,但该系统使用较为复杂,延长了治疗的时间,个别患者不能忍受.     

TFF3作为肿瘤生物标志物的研究

三叶因子3（trefoil factor 3, TFF3）为三叶因子多肽家族成员之一,与肿瘤的发生发展密切相关,可促进肿瘤的侵袭、转移与血管生成。作为肿瘤生物标志物,TFF3对胃癌诊断具有较高的敏感度和特异性,优于胃蛋白酶原（Pepsinogen, PG）标志物,是胃癌非侵入性筛查潜在的理想标志物,并可应用于胃肠道肿瘤化疗药效与预后的评价,同时,TFF3应用于子宫内膜样腺癌及甲状腺微小浸润性滤泡癌的病理诊断也具有重大临床价值。TFF3作为新型肿瘤生物标志物,在肿瘤分子诊断与靶向、个体化治疗领域倍受临床关注。