生存素反义寡脱氧核苷酸对人胃癌细胞株凋亡的影响

背景：生存素（survivin）是凋亡抑制蛋白（IAP）基因家族成员之一，在多数肿瘤组织中高表达。目的：观察生存素反义寡脱氧核苷酸（ASODN）对人胃癌细胞株凋亡的影响。方法：将体外培养的人胃癌细胞株SGC-7901分为不同浓度生存素ASODN组、无关寡脱氧核苷酸（N-ODN）组和对照组。以四甲基偶氮唑蓝（MTT）试验检测生存素ASODN对SGC-7901细胞生长的影响；通过形态学观察、DNA电泳和流式细胞仪分析反映细胞凋亡情况；以端粒重复序列扩增-酶联免疫吸附测定（TRAP-ELISA）方法检测端粒酶活性。结果：生存素ASODN能抑制SGC-7901细胞生长，诱导细胞凋亡，抑制端粒酶活性。凋亡细胞形态学上表现为细胞膜起泡、染色质固缩、核碎裂、凋亡小体形成；DNA电泳呈现凋亡特征性阶梯状条带；流式细胞仪分析显示G1期前出现亚二倍体凋亡峰。结论：生存素ASODN能诱导人胃癌细胞株SGC-7901凋亡，抑制细胞生长及其端粒酶活性。     

人端粒酶反义寡脱氧核苷酸对胃癌细胞系SGC-7901的生长抑制和诱导凋亡的研究

背景端粒酶活性在胃癌组织中表达率很高,在正常胃黏膜组织中则基本不表达.因此,以端粒酶为靶点的反义治疗有望成为胃癌治疗的有效途径之一.目的检测特定的人端粒酶反义寡脱氧核苷酸(AS-ODN)对胃癌细胞系SGC-7901生长的抑制作用,并证明其主要机制为抑制端粒酶活性和诱导细胞凋亡.方法用改良的聚合酶链反应(PCR)-端粒重复扩增协议(TRAP)法定量检测端粒酶AS-ODN作用前后SGC-7901细胞的端粒酶活性;台盼蓝染色法观察SGC-7901细胞活力;光镜和电镜观察凋亡细胞形态,流式细胞仪检测细胞凋亡.结果SGC-7901细胞有端粒酶活性表达.不同浓度的端粒酶AS-ODN作用于SGC-7901细胞48～96 h后,细胞端粒酶活性和生长受到明显抑制,光镜、电镜观察和流式细胞仪检测均证实有细胞凋亡存在.错义AS-ODN(N-ODN)处理组SGC-7901细胞则无显著变化(P＜0.05).结论端粒酶AS-ODN通过抑制胃癌细胞的端粒酶活性和诱导细胞凋亡,最终抑制胃癌细胞生长,其抑制作用呈剂量、时间依赖性和序列特异性.端粒酶AS-ODN对端粒酶活性的抑制比对细胞生长的抑制更敏感,两种抑制作用并不完全平行.     

抗Fas单克隆抗体诱导人胃癌细胞系SGC-7901细胞凋亡

目的探讨抗Fas单克隆抗体诱导胃癌细胞凋亡的规律及在胃癌治疗中的意义.方法应用细胞形态观察、琼脂糖凝胶电泳、流式细胞光度术检测抗Fas 单克隆抗体对胃癌细胞SGC-7901增殖周期的影响以及对细胞杀伤作用的方式,并检测了SGC -7901细胞表面Bcl-2的表达情况..结果抗Fas单克隆抗体有阻滞细胞周期、通过诱发凋亡而抑制肿瘤细胞生长的作用. 经抗Fas单克隆抗体处理后,SGC-7901细胞表面Bcl-2蛋白表达无明显变化. .结论抗Fas单克隆抗体可以诱导胃癌细胞系SGC-7901细胞凋亡. 抗Fas单克隆抗体诱导胃癌细胞凋亡与Bcl-2表达无关.     

萝卜硫素对人胃癌SGC-7901细胞凋亡的影响及其机制研究

目的 研究萝卜硫素对人胃癌SGC-7901细胞凋亡的影响及其可能的作用机制。方法 应用细胞计数试剂盒(CCK-8)检测萝卜硫素对SGC-7901细胞增殖的影响,流式细胞术分析萝卜硫素对SGC-7901细胞周期和凋亡的影响,蛋白免疫印迹法(Western blotting)分析萝卜硫素对SGC-7901细胞中Notch1、Hes1、Bax及Bcl-2蛋白表达的影响。结果 萝卜硫素能够显著抑制SGC-7901细胞的增殖,促使其凋亡,表现出时间和剂量依赖性,萝卜硫素还能将SGC-7901细胞停留在G_1期;萝卜硫素能显著抑制Notch1、Hes1、Bcl-2蛋白表达,诱导促凋亡蛋白Bax表达,与对照组相比,差异均有统计学意义(P0.05)。结论 萝卜硫素可以明显诱导胃癌SGC-7901细胞凋亡,可能通过抑制Notch1/Hes1信号通路、降低Bcl-2/Bax比例实现。     

调控线粒体膜电位青蒿琥酯诱导胃癌SGC-7901细胞凋亡作用

目的研究青蒿琥酯(Art)抑制胃癌细胞(SGC-7901)生长作用机制,探讨Art调控SGC-7901细胞线粒体膜电位诱导SGC-7901细胞凋亡作用与Art抑制胃癌细胞生长作用关系。方法利用流式细胞术(FCM)检测不同浓度的Art干预SGC-7901细胞24 h后的细胞凋亡,细胞线粒体膜电位及细胞中B细胞淋巴瘤(Bcl)-2、B细胞淋巴瘤2相关蛋白(Bax)、半胱氨酸天冬氨酸蛋白酶(Caspase)-3蛋白表达水平。选取Art的浓度为30、60、120μmol/L。对照组使用生理盐水代替Art。结果 FCM检测结果显示,Art组SGC-7901细胞凋亡率显著高于对照组(均P0.05),且Art诱导SGC-7901细胞凋亡作用具有Art剂量依赖性。Art组SGC-7901细胞中Bcl-2蛋白表达水平及细胞线粒体膜电位水平显著低于对照组(P0.05),而SGC-7901细胞中的Bax及Caspase-3蛋白表达量显著高于对照组(均P0.05)。结论 Art具有抑制胃癌SGC-7901细胞生长作用,其作用机制与Art降低SGC-7901细胞线粒体膜电位从而诱导细胞凋亡有关。     

SCH66336对胃癌细胞增殖和凋亡的影响及作用机制

目的探讨法尼基转移酶抑制剂（FTIs）SCH66336对胃癌SGC-7901与MGC-803细胞增殖、凋亡的影响及机制。方法取对数生长期胃癌SGC-7901与MGC-803细胞,分为实验组和对照组,实验组加入SCH66336使终浓度分别为0.1、0.3、1.0、3.0μM,对照组加入含等体积DMSO的培养基,每组设3个复孔。MTT法检测各组细胞增殖抑制率;流式细胞术测定细胞周期与细胞凋亡率,Western blot法检测细胞中核糖体蛋白S6的磷酸化（S235/236）、细胞周期素D1（cyclin D1）与活化的Caspase-3表达情况。结果与对照组比较,SCH66336作用后SGC-7901与MGC-803细胞抑制率及凋亡率明显升高,呈G0/G1细胞周期阻滞,cyclin D1与S6磷酸化表达明显降低、活化的Caspase-3表达升高（P〈0.05）,且呈时间及剂量依赖性。结论 SCH66336对SGC-7901与MGC-803胃癌细胞具有增殖抑制和凋亡诱导作用,其机制可能为抑制S6的活化、下调cyclin D1表达、激活Caspase-3依赖的凋亡通路。     

木黄酮对人胃癌细胞SGC-7901作用的研究

目的探讨木黄酮对体外培养的人胃癌细胞SGC-7901生长的抑制和诱导细胞凋亡的作用。方法用MTT法检测药物效应，透射电镜及流式细胞仪观察木黄酮处理SGC-7901细胞后细胞周期和细胞凋亡。细胞免疫化学观察木黄酮处理SGC-7901细胞后，SGC-7901细胞PCNA，FAS，C-mvc的变化。结果①MTT法证实木黄酮对SGC-7901细胞生长有抑制作用，并呈剂量-效应关系。②流式细胞仪分析木黄酮处理SGC-7901细胞后细胞滞留于G2／M期，并可见凋亡峰。③透射电镜可见SGC-7901细胞出现典型的细胞凋亡及坏死形态学改变。④木黄酮下调PCNA及C—myc表达，上调FAS表达。结论木黄酮对人胃癌细胞SGC-7901有抑制作用，其抑制作用可能通过下调C-mvc基因表达，上调Fas蛋白表达，下调PCNA表达，从而多途径诱导胃癌细胞凋亡和坏死、阻抑细胞周期进程，抑制SGC-7901细胞增殖。     

GRP78在胃癌中表达水平及沉默表达后对人胃癌SGC-7901/DDP细胞增殖和凋亡的影响

目的研究内质网分子伴侣葡萄糖调节蛋白78(glucose regulated protein 78,GRP78)在人不同胃组织(正常胃组织和胃癌组织)和细胞(正常胃上皮GES1细胞、胃癌SGC-7901细胞、多耐药性胃癌SGC-7901/DDP细胞)中的表达水平;揭示GRP78沉默表达对SGC-7901/DDP细胞增殖和凋亡的影响。方法利用实时荧光定量PCR(Real-time PCR)和免疫印迹(Western blotting)方法分别检测人正常胃组织、胃癌组织、人正常胃上皮GES1细胞、胃癌SGC-7901细胞、多耐药性胃癌SGC-7901/DDP细胞中GRP78 mRNA和蛋白表达水平。利用LipfectamineTM2000将GRP78 siRNA转染至SGC-7901/DDP细胞中,同时设置未转染Control组和无义转染Control siRNA组。Real-time PCR和Western blotting方法检测各组SGC-7901/DDP细胞转染效率;MTT方法检测各组SGC-7901细胞的生长活力变化和不同浓度顺铂DDP作用下细胞增殖抑制率;流式细胞术检测各组SGC-7901细胞凋亡情况。结果胃癌组织中GRP78 mRNA和蛋白表达水平显著高于正常胃组织(P0.05);多耐药性胃癌SGC-7901/DDP细胞中GRP78 mRNA和蛋白表达水平显著高于胃癌SGC-7901细胞和正常胃上皮GES1细胞(P0.05);GRP78 siRNA转染SGC-7901/DDP细胞后GRP78 mRNA和蛋白表达水平显著下降(P0.05);与Control组和Control siRNA组相比,GRP78 siRNA转染组SGC-7901/DDP细胞生长活力显著下降,DDP作用下细胞增殖抑制率和细胞凋亡率显著增加(P0.05)。结论 GRP78 mRNA和蛋白在胃癌组织中高表达,在多耐药性胃癌SGC-7901/DDP细胞中也高表达,证实GRP78在胃癌中发挥促癌基因的作用。而GRP78 siRNA转染能够沉默SGC-7901/DDP细胞中GRP78基因表达,抑制SGC-7901/DDP细胞增殖并促进细胞凋亡。     

基因沉默血管内皮生长因子受体3对胃癌细胞增殖的抑制作用

目的: 探讨靶向血管内皮生长受体-3(vascularendothelial growth factor receptor-3, VEGFR-3)小干扰RNA重组载体对胃癌细胞增殖的作用.方法: 构建pSUPER-shRNA/VEGFR3重组载体, 将其转染入胃癌细胞SGC-7901, 采用MTT法观察细胞的生长曲线, RT-PCR检测重组载体在转染前后VEGFR-3 mRNA表达水平的变化, Western blot检测VEGFR-3的蛋白表达.结果: pSUPER-shRNA/VEGFR3重组载体可显著抑制SGC-7901细胞中VEGFR-3基因的表达( P<0.05); 转染pSUPER-shRNA/VEGFR3的SGC-7901细胞生长明显受抑制( P<0.05),VEGFR-3基因蛋白表达明显降低( P<0.05).结论: pSUPER-shRNA/VEGFR3重组载体能够对胃癌细胞SGC-7901中VEGFR-3形成基因沉默, 并抑制胃癌细胞的增殖.     

三氧化二砷诱导胃癌细胞凋亡及其对C-myc和TGF-β1表达的影响

目的 探讨三氧化二砷（As2O3）对体外培养的人胃癌细胞SGC-7901生长的抑制和诱导细胞凋亡的作用。方法 用MTT法检测药物效应，透射电镜及流式细胞仪观察As2O3处理SGC-7901细胞后细胞周期细胞凋亡。细胞免疫化学观察As2O3处理后SGC-7901细胞TGF-β1及C-myc表达的变化。结果 ①MTT法证实As2O3对SGC-7901细胞生长有抑制作用，并呈剂量．效应关系。②流式细胞仪分析As2O3处理SGC-7901细胞后细胞滞留于G2／M期，并可见凋亡峰。③透射电镜可见SGC-7901细胞出现典型的细胞凋亡及坏死形态学改变。④As2O3导致C—myc表达的波动，下调TGF-β1，表达。结论As203对人胃癌细胞SGC-7901有抑制作用，其抑制作用可能通过导致C—myc基因表达波动，诱导胃癌细胞凋亡和坏死、阻抑细胞周期进程，抑制SGC-7901细胞增殖。同时通过下调TGF-β1表达阻止胃癌的恶性进程。     

Effect of NF-κB, survivin, Bcl-2 and Caspase3 on apoptosis of gastric cancer cells induced by tumor necrosis factor related apoptosis inducing ligand

AIM: To study the effect of NF-κB, survivin, Bd-2 and Caspase3 on tumor necrosis factors related apoptosis inducing ligand (TRAIL) induced apoptosis of gastric cancer cells. METHODS: Gastric cancer cells of SGC-7901, MKN28, MKN45 and AGS lines were cultured in PRMI-1640 medium and the apoptosis rates of the cells of 4 lines were observed after treatment of tumor necrosis factors related apoptosis indudng ligand (TRAIL) with a flow cytometer. The expression of NF-κB, survivin, Bcl-2 and Caspase3 in gastric cancer cells of 4 lines was analyzed with Western blot. RESULTS: After the gastric cancer cells were exposed to TRAIL 300 ng/ml for 24 hours, the apoptosis rate was 36.05%, 20.27%, 16.50% and 11.80% in MKN28, MKN45,AGS and SC-C-7901cells respectively. Western blot revealed that the expressions of NF-EB and survivin were lower in MKN28 cells than in MKN45, AGS and SGC-7901 cells. In contrast, the expression of Caspase3 was higher in MKN28 cells than in MKN45, AGS and SGC-7901 cells. CONCLUSION: There is a selectivity of TRAIL potency to induce apoptosis in gastric cancer cells of different cell lines.The anticancer potency of TRAIL is associated with the decreased expression of NF-κB and survivin and increased expression of Caspase3 of gastric cancer cells.     

Synergistic effect of oxymatrine and angiogenesis inhibitor NM-3 on modulating apoptosis in human gastric cancer cells

AIM: To investigate the synergistic effect of oxymatrine(OM) and angiogenesis inhibitor NM-3 on modulatingapoptosis in human gastric cancer cell lines SGC-7901,MKN-45, MKN-74. METHODS: Human gastric cancer lines SGC-7901,MKN-45, MKN-74 were treated with OM in the absenceand presence of NM-3. The inhibitory rates weredetected by MTT assay. Synergistic effect of OM andNM-3 on the growth of survivin, bcl-2, bax and p53 inSGC-7901 cells were examined by semiquantitative RT-PCR and Western blotting, and their growth inhibitoryeffects were also observed on SGC-7901 tumor xenograftin nude mice.RESULTS: OM combined with NM-3 exhibited asynergistic inhibitory effect on the growth of SGC-7901,MKN-45 and MKN-74 cells in a time-dependent manner.Twenty-four hours after treatment with OM, NM-3 aloneand their combination, mRNA expression of survivin andbcl-2 in SGC-7901 cells decreased, p53 mRNA expressionincreased. OM (4 g/L) combined with NM-3 significantlyincreased the expression of p53 mRNA and decreasedthe expression of survivin and bcl-2 compared witheither agent alone (193% ± 34% vs 129% ± 12%;44% ± 18% vs 92% ± 18%; 36 ± 17% vs 93% ± 23%,P < 0.05). Western blotting showed that the synergisticeffect of OM and NM-3 on protein translation of survivin,bcl-2 and p 53 was in accordance with their mRNAs.Furthermore, OM/NM-3 combination obviously exhibitedantitumor growth effect in xenografted human gastriccancer cells SGC-7901 compared with either agent alone.CONCLUSION: OM combined with NM-3 has synergisticinhibitory effects on human gastric cancer cells in vitro and can suppress the growth of xenografted human gastric cancer cells SGC-7901 in vivo.     

Effect of NF-κB, survivin, Bcl-2 and Caspase3 on apoptosis of gastric cancer cells induced by tumor necrosis factor related apoptosis inducing ligand

AIM: To study the effect of NF-κB, survivin, Bcl-2 and Caspase3 on tumor necrosis factors related apoptosis inducing ligand (TRAIL) induced apoptosis of gastric cancer cells.METHODS: Gastric cancer cells of SGC-7901, MKN28,MKN45 and AGS lines were cultured in PRMI-1640 medium and the apoptosis rates of the cells of 4 lines were observed after treatment of tumor necrosis factors related apoptosis inducing ligand (TRAIL) with a flow cytometer. The expression of NF-κB, survivin, Bcl-2 and Caspase3 in gastric cancer cells of 4 lines was analyzed with Western blot.RESULTS: After the gastric cancer cells were exposed to TRAIL 300 ng/ml for 24 hours, the apoptosis rate was 36.05%, 20.27%, 16.50% and 11.80% in MKN28, MKN45,AGS and SGC-7901cells respectively. Western blot revealed that the expressions of NF-κB and survivin were lower in MKN28 cells than in MKN45, AGS and SGC-7901 cells. In contrast, the expression of Caspase3 was higher in MKN28 cells than in MKN45, AGS and SGC-7901 cells.CONCLUSION: There is a selectivity of TRAIL potency to induce apoptosis in gastric cancer cells of different cell lines.The anticancer potency of TRAIL is associated with the decreased expression of NF-κB and survivin and increased expression of Caspase3 of gastric cancer cells.     

Tributyrin inhibits human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesis arrest

AIM: To evaluate the effects of tributyrin, a pro-drug of natural butyrate and a neutral short-chain fatty acid triglyceride, on the growth inhibition of human gastric cancer SGC-7901 cell.METHODS: Human gastric cancer SGC-7901 cells were 24-72 h. MTT assay was applied to detect the cell proliferation.[3H]-TdR uptake was measured to determine DNA synthesis.Apoptotic morphology was observed by electron microscopy and Hoechst-33258 staining. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect tributyrin-triggered apoptosis. The expressions of PARP, Bcl-2 and Bax were examined by Western blot assay.RESULTS: Tributyrin could initiate growth inhibition of SGC7901 cell in a dose- and time-dependent manner. [3H]-TdR uptake by SGC-7901 cells was reduced to 33.6% after 48 h control (P＜0.05). Apoptotic morphology was detected by TUNEL assay. Flow cytometry revealed that tributyrin could induce apoptosis of SGC-7901 cells in dose-dependent manner. After 48 hours incubation with tributyrin at 2 mmol.L-1, the level of Bcl-2 protein was lowered, and the level of Bax protein was increased in SGC-7901, accompanied by PARP cleavage.CONCLUSION: Tributyrin could inhibit the growth of gastric cancer cells effectively in vitro by inhibiting DNA synthesis and inducing apoptosis, which was associated with the downregulated Bcl-2 expression and the up-regulated Bax expression. Therefore, tributyrin might be a promising chemopreventive and chemotherapeutic agent against human gastric carcinogenesis.     

AG490对胃癌细胞株SGC-7901细胞周期、凋亡和STAT3表达的影响

背景：JAK2酪氨酸激酶特异性抑制剂AG490可抑制胃癌细胞生长,但目前对其作用机制还知之甚少。目的：探讨AG490对胃癌细胞株SGC-7901细胞周期、凋亡和STAT3 mRNA表达的影响。方法：以不同浓度AG490处理胃癌细胞株SGC-7901,流式细胞术检测细胞周期和凋亡情况,RT-PCR法检测STAT3 mRNA表达。结果：胃癌细胞株SGC-7901经AG490作用48 h后,100μmol/L组的S期、G2/M期细胞比例显著增加（P〈0.01）,1μmol/L组和10μmol/L组仅G2/M期细胞比例显著下降（P〈0.05）。AG490作用48h后,各浓度组的细胞凋亡率均显著增加（P〈0.01）。AG490作用24 h和48 h后,各浓度组的STAT3 mRNA表达均无明显变化（P〉0.05）。结论：AG490可影响胃癌细胞株SGC-7901的细胞周期并诱导细胞凋亡,但不影响STAT3 mRNA的表达。     

Tributyrin inhibits human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesis arrest

AIM: To evaluate the effects of tributyrin, a pro-drug of natural butyrate and a neutral short-chain fatty acid triglyceride, on the growth inhibition of human gastric cancer SGC-7901 cell. METHODS: Human gastric cancer SGC-7901 cells were exposed to tributyrin at 0.5, 1, 2, 5, 10 and 50 mmol/L(-1) for 24-72 h. MTT assay was applied to detect the cell proliferation. [(3)H]-TdR uptake was measured to determine DNA synthesis. Apoptotic morphology was observed by electron microscopy and Hoechst-33258 staining. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect tributyrin-triggered apoptosis. The expressions of PARP, Bcl-2 and Bax were examined by Western blot assay. RESULTS: Tributyrin could initiate growth inhibition of SGC-7901 cell in a dose- and time-dependent manner. [(3)H]-TdR uptake by SGC-7901 cells was reduced to 33.6 % after 48 h treatment with 2 mmol/L(-1) tributyrin, compared with the control (P<0.05). Apoptotic morphology was detected by TUNEL assay. Flow cytometry revealed that tributyrin could induce apoptosis of SGC-7901 cells in dose-dependent manner. After 48 hours incubation with tributyrin at 2 mmol/L(-1), the level of Bcl-2 protein was lowered, and the level of Bax protein was increased in SGC-7901, accompanied by PARP cleavage. CONCLUSION: Tributyrin could inhibit the growth of gastric cancer cells effectively in vitro by inhibiting DNA synthesis and inducing apoptosis, which was associated with the down-regulated Bcl-2 expression and the up-regulated Bax expression. Therefore, tributyrin might be a promising chemopreventive and chemotherapeutic agent against human gastric carcinogenesis.     

Therapeutic mechanism of ginkgo biloba exocarp polysaccharides on gastric cancer

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 SGC-7901 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-fos 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-fos genes, which can inhibit proliferation and induce apoptosis and differentiation of tumor cells.     

强力霉素对胃癌细胞SGC-7901基质金属蛋白酶-2和基质金属蛋白酶组织抑制因子-2表达的影响

背景：强力霉素对结肠癌细胞的分化和抑制作用已有报道，但其对胃癌细胞的作用尚未见报道。目的：观察强力霉素对人胃癌细胞SGC-7901的生长抑制作用及其对基质金属蛋白酶（MMP）-2和基质金属蛋白酶组织抑制因子（TIMP）-2表达的影响，探索胃癌治疗的新方法。方法：采用不同浓度的强力霉素作用于胃癌细胞SGC-7901，以噻唑蓝（MIT）法测定其细胞毒作用；逆转录聚合酶链反应（RT—PCR）法半定量测定MMP．2和TIMP-2mRNA的表达；免疫组化法观察MMP-2蛋白的表达。结果：强力霉素可抑制胃癌细胞SGC-7901的生长，具有浓度和时间依赖性（P〈0．01）。强力霉素可下调MMP-2mRNA和MMP-2蛋白的表达，上调TIMP-2mRNA的表达，具有浓度依赖性（P〈0．05）。结论：强力霉素能抑制胃癌细胞SGC-7901的生长，其作用机制可能与下调MMP-2表达、上调TIMP-2表达有关。     

Paclitaxel induces apoptosis in human gastric carcinoma cells

AIM: To investigate the apoptosis in gastric cancer cells induced by paclitaxel, and the relation between this apoptosis and expression of Bcl-2 and Bax. METHODS: In in vitro experiments, MTT assay was used to determine the cell growth inhibitory rate. Transmission electron microscope and TUNEL staining method were used to quantitatively and qualitively detect the apoptosis status of gastric cancer cell line SGC-7901 before and after the paclitaxel treatment. Immunohistochemical staining was used to detect the expression of apoptosis-regulated gene Bcl-2 and Bax. RESULTS: Paclitaxel inhibited the growth of gastric cancer cell line SGC-7901 in a dose-and time-dependent manner. Paclitaxel induced SGC-7901 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation, nucleus fragmentation and apoptotic body formation. Paclitaxel could reduce the expression of apoptosis-regulated gene Bcl-2, and improve the expression of apoptosis-regulated gene Bax. CONCLUSION: Paclitaxel is able to induce the apoptosis in gastric cancer. This apoptosis may be mediated by down-expression of apoptosis-regulated gene Bcl-2 and up-expression of apoptosis-regulated gene Bax.