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| 1 | Effects of hydroxyapatite nanoparticles on proliferation and apoptosis of human hepatoma BEL-7402 cells显示文摘AIM: To study the effect of hydroxyapatite (HAP) nanoparticleson human hepatoma cell line BEL-7402 in vitro.METHODS: The human hepatoma cell line BEL-7402 wascultured and treated with HAP nanoparticles at variousconcentrations. Growth suppression was detected with MTTcolorimetric assay, cell apoptotic alterations were evaluatedby cytochemical staining (Hoechst 33258), transmissionelectron microscopy (TEM), and flow cytometry (FCM).RESULTS: HAP nanoparticles inhibited the growth ofhepatoma cells in a dose-dependent manner, with IC50 valuesof 29.30 mg/L. Treated with 50-200 mg/L HAP nanoparticlesfor 48 h, BEL-7402 cells apoptosis with nuclear chromatincondensation and fragmentation as well as cell shrinkageand the formation of apoptotic bodies were observed undercytochemical staining and transmission electron microscopy.FCM analysis showed hypodiploid peaks on histogram, theapoptotic rates at the concentrations of 50, 75, 100, 150and 200 mg/L of HAP nanoparticles were 20.35±2.23%,25.35±1.92%, 29.34±4.61%, 44.92±3.78 % and53.64±3.49%, respectively, which were all significantlyhigher than that of control group 2.23±0.14%. There wasa significant correlation between HAP nanoparticleconcentration and apoptotic rate (r=0.994, P<0.01).CONCLUSION: HAP nanoparticles not only inhibitproliferation but also induce apoptosis of human hepatoma cell line BEL-7402 in vitro. | Zhi-Su Liu Sheng-Li Tang Zhong-Li Ai Department of General Surgery,Zhongnan Hospital of Wuhan University,Wuhan 430071,Hubei Province,China | 2003 | World Journal of Gastroenterology2003，9，9： | 33 |
| 2 | PPARγ pathway activation results in apoptosis and COX-2 inhibition in HepG2 cells显示文摘AIM: To investigate whether troglitazone (TGZ), theperoxisome proliferator-activated receptor (PPAR) gammaligand, can induce apoptosis and inhibit cell proliferation inhuman liver cancer cell line HepG2 and to explore themolecular mechanisms.
METHODS: [3-(4,5)-dimethyithiazol-2-yl]-2,5-diphenyltetrazolium bromide (NTT), [3H] Thymidine incorporation,Hochest33258 staining, DNA ladder, enzyme-linkedimmunosorbent assay (ELISA), RT-PCR, Northern and Western blotting analyses were employed to investigate the effect of TGZ on HepG2 cells and related molecular mechanisms.RESULTS: TGZ was found to inhibit the growth of HepG2cells and to induce apoptosis. During the process, the expression of COX-2 mRNA and protein and Bcl-2 protein was down-regulated, while that of Bax and Bak proteins was up-regulated, and the activity of caspase-3 was elevated.Furthermore, the level of PGE2 was decreased transiently after 12 h of treatment with 30 gM troglitazone.
CONCLUSION: TGZ inhibits cell proliferation and induces apoptosis in HepG2 cells, which may be associated with the activation of caspase-3-like proteases, down-regulation of the expression of COX-2 mRNA and protein, Bcl-2 protein,the elevation of PGE2 levels, and up-regulation of the expressions of Bax and Bak proteins. | Ming-YiLi HuaDeng Jia-MingZhao DongDai Xiao-YuTan | 2003 | World Journal of Gastroenterology2003，9，6： | 25 |
| 3 | Therapeutic mechanism of ginkgo biloba exocarp polysaccharides on gastric cancer显示文摘AIM: To study the therapeutic mechanism of Ginkgo biloba exocarp polysaccharides (GBEP) on gastric cancer.METHODS: Thirty patients with gastric cancer were treated with oral GBEP capsules. The area of tumors was measured by electron gastroscope before and after treatment, then the inhibitory and effective rates were calculated. The ultrastructures of tumor cells were examined by transmissional electron microscope. Cell culture, MTT, flow cytometry were performed to observe proliferation, apoptosis and changes of relevant gene expression of human gastric cancer SGC-7901 cells.RESULTS: Compared with the statement before treatment,GBEP capsules could reduce the area of tumors, and the effective rate was 73.4 %. Ultrastructural changes of the cells indicated that GBEP could induce apoptosis and differentiation in tumor cells of patients with gastric cancer.GBEP could inhibit the growth of human gastric cancer SGC7901 cells following 24-72 h treatment in vitro at 10-320 mg/L,which was dose- and time-dependent. GBEP was able to elevate the apoptosis rate and expression of c-los gene,but reduce the expression of c-myc and bcl-2 genes also in a dose-dependent manner.CONCLUSION: The therapeutic mechanism of GBEP on human gastric cancer may relate to its effects on the expression of c-myc, bcl-2 and c-los genes, which can inhibit proliferation and induce apoptosis and differentiation of tumor cells. | Ai-HuaXu Hua-ShengChen Bu-ChanSun Xiao-RenXiang Yun-FeiChu FanZhai Ling-ChangJia | 2003 | World Journal of Gastroenterology2003，9，11： | 21 |
| 4 | Peroxisome proliferator-activated receptor gamma ligands inhibit cell growth and induce apoptosis in human liver cancer BEL-7402 cells显示文摘AIM: To investigate the characteristics of PPAR gamma ligands induced apoptosis in liver cancer cells.METHODS: The effects of ligands for each of the PPAR gamma ligands on DNA synthesis and cell viability were examined in BEL-7402 liver cancer cells. Apoptosis was characterized by Hochest33258 staining, DNA fragmentation,TUNEL and ElISA, and cell cycle kinetics by FACS. Modulation of apoptosis related caspases expression by PPAR gamma ligands was examined by Western blot.RESULTS: PPARgamma ligands, 15-deoxy-12,14-prostaglandin J2 (15d-PGJ2) and troglitazone (TGZ), suppressed DNA synthesis of BEL-7402 cells. Both 15d-PGJ2 and TGZ induced BEL-7402 cell death in a dose dependent manner, which was associated with an increase in fragmented DNA and TUNEL-positive cells. At concentrations of 10 and 30 μM,15d-PGJ2 or troglitazone increased the proportion of cells with G0/G1 phase DNA content and decreased those with S phase DNA content. There was no significant change in the proportion of cells with G2/M DNA content. The activities of Caspases-3, -6, -7 and -9 were increased by 15d-PGJ2and TGZ treatment, while the activity of Caspase 8 had not significantly changed.CONCLUSION: The present results suggest the potential usefulness of PPAR gamma ligands for chemoprevention and treatment of liver cancers. | Ming-YiLi HuaDeng .lia-MingZhao DongDai Xiao-YuTan | 2003 | World Journal of Gastroenterology2003，9，8： | 16 |
| 5 | Apoptosis of hepatoma cells SMMC-7721 induced by Ginkgo biloba seed polysaccharide显示文摘AIM: To study the apoptosis of hepatoma cells SMMC-7721induced by polysaccharide isolated from Ginkgo biloba seed.METHODS: Ginkgo biloba seed polysaccharide (GBSP) wasisolated by ethanol fractionation of Ginkgo biloba seed andpurified by Sephadex G-200 chromatography. The purity ofGBSP was verified by reaction with iodine-potassium iodideand ninhydrin and confirmed by UV spectrophotometer,cellulose acetate membrane electrophoresis and Sepharose4B gel filtration chromatography. The Scanning ElectronMicroscope (SEM) and Flow Cytometrv (FCM) were used toexamine the SMMC-7721 cells with and without GBSPtreatment at 500 mg/ml for 36 h.RESULTS: GBSP product obtained was of high purity withthe average molecular weight of 1.86 × 105. Quantitativeanalysis of SMMC-7721 cells in vitro with FCM showed thatthe percentages of G2-M cells without and with GBSPtreatment were 17.01±1.28 % and 11.77±1.50% (P<0.05),the debds ratio of the cells were 0.46±0.12 % and 0.06±0 .06 %(P<0.01), and the apoptosis ratio of cells was 3.84±0 .55 %and 9.13±1.48 %(P<0.01) respectively. Following GBSPtreatment, microvilli of SMMC-7721 cells appeared thinnerand the number of spherical cells increased markedly. Mostsignificantly, the apoptosis bodies were formed on andaround the spherical cells treated with GBSP.CONCLUSION: GBSP could potentially induce the apoptosisof SMMC-7721 cells. | Gui-Wen Yang Li-Guo An Department of Biology,Shandong Normal University,Jinan 250014,Shandong Province,China Qun Chen Department of Biology & Chemistry,Huainan Teachers College,Huainan 232001,Anhui Province,China | 2002 | World Journal of Gastroenterology2002，8，5： | 15 |
| 6 | Degradation of retinoid X receptor α by TPA through proteasome pathway in gastric cancer cells显示文摘AIM: To investigate and determine the mechanism and signal pathway of tetradecanoylphorbol-1, 3-acetate (TPA) in degradation of RXRα.METHODS: Gastric cancer cell line, BGC-823 was used in the experiments. The expression level of R XRα protein was detected by Western blot. Nuclear and cytoplasmic protein fractions were prepared through lysis of cell and centrifugation.Localization and translocation of RXRα were observed under laser-scanning confocal microscope through labeling specific anti-RXRα antibody and corresponding immunofiuorescent antibody as secondary antibody. Different inhibitors were used as required.RESULTS: In BGC-823 cells, RXRα was expressed in the nucleus. When cells were treated with TPA, expression of RXRα was repressed in a time-dependent and TPAconcentration-dependent manner. Meanwhile, translocation of RXR from the nucleus to the cytoplasm occurred, also in a time-dependent manner. When cells were pre-incubated with proteasome inhibitor MG132 for 3 hrs, followed by TPA for another 12 hrs, TPA-induced RXRα degradation was inhibited. Further observation of RXRα translocation in the presence of MG132 showed that MG-132 could block TPAinduced RXRα redistribution. Conversely, when RXRαtranslocation was inhibited by LMB, an inhibitor for blocking protein export from the nucleus, TPA could not repress expression of RXRα.CONCLUSION: TPA could induce the degradation of RXRα protein in BGC-823 cells, and this degradation is time-and TPA-concentration-dependent. Furthermore, the degradation of RXRα by TPA is via a proteasome pathway and associated with RXRα translocation from the nucleus to the cytoplasm. | Xiao-Feng Ye Su Liu Qiao Wu Xiao-Feng Lin Bing Zhang Jia-Fa Wu Ming-Qing Zhang Wen-Jin Su Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering,School of Life Sciences,Xiamen University,Xiamen 361005,Fujian Province,China | 2003 | World Journal of Gastroenterology2003，9，9： | 6 |
| 7 | 槲皮素联合顺铂对胃癌SGC-7901细胞增生和凋亡的影响显示文摘目的:探讨槲皮素(quercetin,QU)联合顺铂(DDP)对胃癌SGC-7901细胞增生、凋亡及凋亡相关基因Bcl-XL mRNA表达的影响. 方法:用槲皮素和顺铂处理胃癌SGC-7901细胞后,应用光镜、电镜、MTT法、流式细胞仪和RT-PCR 技术研究胃癌细胞的形态学变化、生长抑制、诱导凋亡和对凋亡相关基因Bcl-XL mRNA表达的影响. 结果:药物作用于细胞24 h后,可看到较为典型的细胞凋亡形态学变化.DDP和QU均可以抑制胃癌SGC-7901 细胞增生或诱导其凋亡,且有时间和剂量依赖效应,联合应用具有协同效应.联合组的诱导凋亡率及增生抑制效应显著高于单用DDP组(P<0.01),干预48 h后,Bcl- XLmRNA的表达下调,QU可以加强下调作用. 结论:人胃癌SGC-7901细胞体外实验中,QU和顺铂可以抑制其增生并诱导凋亡,二者联合应用有一定的协同效应,且呈剂量依赖关系. | 王海忠 王沁 | 2005 | 世界华人消化杂志2005，13，3： | 6 |
| 8 | 孤儿核受体Nur77的多功能性及其相关药物靶点作用机制的研究进展显示文摘核受体Nur77(也称TR3)是立早基因NR4A1编码的产物,在细胞增殖、分化、凋亡、自噬、炎症以及代谢等生命活动过程中发挥重要的调控作用.Nur77不仅作为转录因子调控下游靶基因的转录和表达,还能作为不依赖于转录的调节因子,通过蛋白相互作用以及改变亚细胞定位的方式发挥作用.Nur77的配体至今尚未在生物体内发现,因此它被称为孤儿核受体.然而,近年的研究已发现数个靶向Nur77并调控其功能的小分子药物.本文重点综述Nur77的多功能性、其体外激动剂和拮抗剂的筛选及其靶向调控的研究进展. | 周波 陈航姿 吴乔 | 2021 | 厦门大学学报(自然科学版)2021，60，2： | 3 |
| 9 | 塞莱西布体外对人类肝胃癌细胞生长的抑制作用显示文摘目的:研究塞莱西布在体外对人类肝癌7721细胞以及胃癌7901细胞的生长抑制作用. 方法:两种肿瘤细胞用含不同浓度(0,20,40,80,160 和320 μmol/L)的塞莱西布的培养液培养.应用MTT测定法来测定生长抑制率,电镜技术来观察细胞凋亡情况,免疫组化技术来检测细胞内Cox-2蛋白含量. 结果:塞莱西布对两种肿瘤细胞均具有生长抑制作用(塞莱西布320μmol/L时两种肿瘤细胞抑制率分别为49.1%和42.9%), 并呈现量-效关系.电镜下可观察到凋亡细胞.免疫组化发现细胞内环氧化酶的含量在处理前后有明显变化. 结论:在体外,塞莱西布抑制人类肝癌及胃癌细胞生长, 诱导他们产生凋亡,并且该作用与细胞内环氧化酶含量有密切关系. | 樊菁 窦科峰 李开宗 | 2004 | 世界华人消化杂志2004，12，3： | 3 |
| 10 | 胃癌组织bcl-2基因表达与细胞凋亡和增生的关系显示文摘目的:探讨胃癌细胞bcl-2基因表达水平与肿瘤细胞增生活性及细胞凋亡程度的关系. 方法:胃癌组织53例,用原位杂交及免疫组化染色法分别检测bcl-2 mRNA,bcl-2蛋白和增生细胞核抗原(PCNA) 的表达,并采用凋亡细胞原位检测方法对组织切片中的凋亡细胞进行观察和比较. 结果:胃癌组织表达bcl-2 mRNA 41例(77.4%),表达Bcl-2 蛋白43例(81.1%),X2检验表明两种方法检测阳性率差异无显著性.胃癌53例增生期细胞标记物PCNA表达及凋亡细胞的阳性率均为100%,细胞凋亡和细胞增生指数呈显著性负相关(r=-0.993,P<0.01).随胃癌细胞Bcl-2蛋白表达水平升高,PCNA阳性细胞指数相应增加,肿瘤凋亡细胞指数则相应减少,Bcl-2蛋白+++组与++组间(t=2.552, 2.699,P<0.05)及前两组分别与-组和+组间(t=4.487, 3.975,2.807,3.094,4.885,5.816,3.404,3.895, P<0.01)凋亡和增生细胞指数差异均有显著性. 结论:胃癌细胞bcl-2基因高表达可引起细胞凋亡减少与过度增生. | 刘海峰 刘为纹 王国安 滕小春 陈刚 汪兴伟 何俊堂 姜利国 | 2004 | 世界华人消化杂志2004，12，11： | 1 |
| 11 | 孤儿受体Nur77与肿瘤的关系显示文摘Nur77作为核受体超家族孤儿受体的一员,同时控制着肿瘤细胞的发生和死亡,与多种肿瘤的发生、发展存在着密切的联系。在细胞核中,Nur77作为致癌的生存因子,促进肿瘤细胞的生长;当其靶向转移到线粒体上与Bcl-2结合并改变Bcl-2的促生长表型,可以触发细胞色素C的释放,从而导致细胞凋亡。阐明Nur77从细胞核靶向转移至线粒体,绑定Bcl-2并改变其表型的机制可能意味着对于那些高度表达Bcl-2的肿瘤能找到新的治疗方法。 | 余小挺 郑亦胡 郑飞云 | 2009 | 肿瘤学杂志2009，15，11： | 1 |
| 12 | Targeting truncated RXRα for cancer therapy显示文摘Retinoid X receptor-alpha (RXR ) ,原子受体总科的一个独特成员,是一个生长得很好的药目标,为癌症为 pharmacologic 干预和治疗学的应用代表最重要的目标之一。不管多么, RXR 怎么并且怎么调整癌症房间生长 RXR 调节的人压制 tumorigenesis 糟糕被理解。改变的表示和 RXR 的异常功能在癌症的开发被含有。以前,几研究证明了 N 严重地截断的 RXR (tRXR ) 蛋白质的存在从 RXR 的有限解朊作用导致了肿瘤房间。最近,我们发现 tRXR 的 overexpression 能由与肿瘤坏死 factor-alpha-induced phosphoinositide 3-kinase 和 NF-B 信号 transduction 小径交往支持肿瘤生长。我们也识别了 nonsteroidal 反煽动性的药 Sulindac 和类似物经由唯一的有约束力的机制的 tRXR 活动的同样有效的禁止者。这评论由在它的表面上指向交替的有约束力的地点在癌症房间幸存和死亡以及发炎和我们 tRXR 规定的最近的理解的规定讨论 tRXR 和调节的人的新兴的角色。 | Xiaokun Zhang Hu Zhou Ying Su | 2016 | Acta Biochimica et Biophysica Sinica2016，48，1： | 1 |
| 13 | 台盼兰染色肿瘤细胞化学药物敏感实验的临床应用价值显示文摘目的:寻找一种简便、易行、费用低廉的肿瘤细胞化疗药物敏感实验方法,并用于指导临床用药。方法:对60例大肠癌患者的癌细胞进行体外有药培养,然后通过台盼兰染色检测细胞活动性的有关指标,确定最佳药物及组合,对病人进行化疗。追踪病人的生存率。结果:实验组的1、2、3、5年生存率分别为96%,83%,70%,43%。对照组的1、2、3、5年生存率分别为93%,73%,60%,33%。具有显著的差异。结论:①该法是一种简便、易行、费用低廉的肿瘤化疗药物敏感实验方法。②该法是具有临床指导价值的方法。 | 杨伟雄 钟华 李定明 林翠芬 谢静誉 张奕文 邱泽成 | 2008 | 河北医学2008，14，1： | 1 |
| 14 | 羟基磷灰石纳米粒子诱导人肝癌细胞凋亡模型的构建显示文摘目的:建立羟基磷灰石纳米粒子体外诱导人肝癌细胞凋亡的模型,为进一步研究纳米粒子诱导肝癌细胞凋亡的分子机制奠定基础.方法:用羟基磷灰石纳米粒子以不同终浓度、不同时间作用于人肝癌BEL—7402细胞,用细胞毒性实验(MTT比色法)观察其细胞毒性,倒置相差显微镜、荧光显微镜、透射电镜、DNA琼脂糖凝胶电泳等方法观察凋亡在形态学和生化方面的变化.流式细胞仪分析以进一步了解凋亡发生的时间和程度.结果:羟基磷灰石纳米粒子以剂量依赖和时间依赖的方式抑制 BEL-7402细胞的生长.50-200 mg/L的纳米粒子处理 48 h后,形态学上,肝癌细胞表现为细胞皱缩、核质浓缩、核碎裂、细胞起泡以及凋亡小体形成等凋亡特征.琼脂糖凝胶电泳观察到DNA“梯带”.流式细胞仪定量分析,0,50、75、100、150、200 mg/L浓度下凋亡率分别为2.2%,20.3%,25.3%,29.8%,45.1%和53.1%.50 mg/L作用 12 h后肝癌细胞出现凋亡,48 h达高峰,12,24,36,48 h 细胞凋亡率分别为 2.7 %,3.5%,6.3%和 21.4%.结论:羟基磷灰石纳米粒子既能抑制人肝癌BEL-7402细胞增生,又能诱导其凋亡,该凋亡模型的成功建立将有助于进一步探讨纳米粒子诱导肝癌细胞凋亡的分子机制. | 刘志苏 唐胜利 艾中立 孙权 钱群 何跃明 朱忠超 | 2003 | 世界华人消化杂志2003，11，9： | 1 |
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