盐酸小檗碱对人腺样囊性癌ACC2细胞增殖及周期的影响

目的研究盐酸小檗碱对人腺样囊性癌ACC2细胞的生长抑制作用和对细胞周期的影响。方法 CCK8法检测不同剂量的盐酸小檗碱对ACC2细胞的增殖抑制作用,并采用流式细胞术分别检测细胞周期及凋亡情况。结果在浓度1～20μg/ml范围内,不同浓度的盐酸小檗碱对人腺样囊性癌ACC2细胞均有抑制作用,且有一定的浓度依赖性。盐酸小檗碱细胞浓度为4.00、7.50及12.13μg/ml作用24 h后,ACC2细胞在S期比例增多,凋亡率明显增加。结论盐酸小檗碱通过干预细胞周期和凋亡对人腺样囊性癌ACC2细胞的增殖起抑制作用,同时与药物浓度有一定的依赖性。     

花青素对NCI-H460细胞的增殖抑制与诱导凋亡作用

目的研究花青素对大细胞型肺癌NCI-H460细胞的增殖抑制和诱导凋亡作用。方法体外培养NCI-H460细胞与25—200μg/ml的花青素共孵育,采用噻唑兰（MTT）法检测细胞增殖抑制率,Hoechst33258荧光染色观察细胞形态,DNA琼脂糖凝胶电泳检测细胞凋亡情况,流式细胞术检测细胞的凋亡率和细胞周期的分布。结果花青素在25—200μg／ml浓度范围内抑制NCI-H460细胞的增殖,有剂量和时间依赖性,花青素对NCI-H460细胞的IC50值为90．8μg／ml,50—200μg／ml的花青素处理NCI-H460细胞72h,Hoechest33258荧光染色可观察到核浓缩及核碎裂等细胞凋亡特征;DNA琼脂糖凝胶电泳有典型的梯形条带;流式细胞图上可看到“亚G1期”凋亡峰,25、50、100、200μg/ml花青素对NCI-H460细胞凋亡率为1．3％、2．0％、11．7％和27．8％,G0／G1细胞数目显著增多,S期细胞显著减少。结论花青素能抑制NCI-H460细胞的增殖,诱导细胞的凋亡,呈剂量依赖性,并使细胞阻滞于G0／G1期。     

藤梨根提取物对人胃癌SGC7901细胞增殖抑制的影响

目的研究藤梨根提取物对胃癌细胞SGC7901的抑制作用及其机制。方法用MTT法检测不同剂量的藤梨根提取物对人胃癌细胞SGC7901的增殖抑制作用,并用流式细胞仪分别检测细胞周期以及凋亡程度。结果在浓度范围25~200μg/ml范围内,不同浓度的藤梨根提取物对胃癌细胞SGC7901均有抑制作用,且有一定的浓度依赖性。且在藤梨根提取物细胞浓度为53、86以及142μg/ml作用48 h后SGC7901在S期比例增多,凋亡率明显增加。结论藤梨根提取物可能通过干预细胞周期和凋亡对胃癌细胞SGC7901增殖起抑制作用,同时与药物浓度有一定的依赖性。     

健脾益气方含药血清对人胃癌细胞株MKN-28凋亡的影响

目的观察健脾益气方含药血清对人胃癌细胞株MKN-28凋亡的影响。方法采用健脾益气方含药血清培养MKN-28,分别在培养24、48、72 h时采用MTT法测算MKN-28增殖抑制率;采用激光共聚焦法及流式细胞术观察MKN-28细胞形态和细胞周期变化。结果健脾益气方含药血清可显著抑制MKN-28增殖,且抑制率与含药血清浓度及其作用时间呈正相关;含药血清可改变MKN-28细胞周期,诱导其凋亡。结论健脾益气方含药血清对人胃癌细胞株MKN-28具有抑制增殖、促进凋亡的作用。     

丁酸钠对人胃癌MKN-28细胞增殖的抑制作用及其机制

目的 观察脱乙酰化酶抑制剂丁酸钠对人胃癌MKN-28细胞增殖的抑制作用,并探讨其作用机制.方法 MTT法观察丁酸钠对人胃癌MKN-28细胞的生长抑制作用;流式细胞术检测细胞凋亡及细胞周期;RT-PCR检测丁酸钠作用前后p21WAF1 mRNA的表达.结果 1.0、2.5、5.0 mmol/L丁酸钠作用24、48、72 h均可抑制 MKN-28细胞增殖,其效果具有时间、剂量依赖性(P＜0.05);丁酸钠1.0、2.5、5.0 mmol/L处理72 h后,MKN-28细胞G0/G1期细胞数量显著增加,S期细胞数量显著降低(P＜0.05);细胞凋亡率分别为13.7%±0.8%、20.8%±2.4%、33.6%±2.6%,与对照组2.8%±0.4%相比P均＜0.05;与对照组比较,丁酸钠处理后p21WAF1 转录水平上调.结论 丁酸钠可显著抑制人胃癌MKN-28细胞的生长,其可能的机制是通过上调p21WAF1基因的表达,诱导细胞凋亡,使细胞周期阻滞于G0/G1期.     

药物诱导胃癌细胞凋亡的初步探索

目的:了解羟基喜树碱和氧化砷体外诱导胃癌细胞凋亡的能力.探索最佳诱导时间和剂量.并初步阐明其作用机制。方法:利用HE染色法、流式细胞仪和DNA末端原位标记染色法(TUNEL)观察羟基喜树碱和氧化砷在体外对胃癌细胞MKN-28(高分化腺癌)。SGC-7901(中分化腺癌)。MKN-45(低分化腺癌)的作用 结果:药物作用48小时后,羟基喜树碱0.01mg/ml组胃癌细胞MKN-28、SGC-7901、MKN-45的凋亡率分别为30.26％、21.88％和12.35％,氧化砷10μmol/L组胃癌细胞MKN-28、SGC-7901、MKN-45的凋亡率分别为22.52％、13.83％和9.68％其中羟基喜树碱在细胞周期的S期诱导胃癌细胞发生凋亡,而氧化砷则主要作用于G2/M期。     

奥曲肽对胃癌细胞增殖和凋亡的作用

[目的]观察奥曲肽对胃癌细胞增殖、凋亡、细胞周期的影响,探讨奥曲肽抑癌的可能作用机制。[方法]应用MTT方法检测不同浓度奥曲肽在不同时间对胃癌BGC823细胞的生长抑制作用;采用流式细胞技术检测奥曲肽对胃癌BGC823细胞周期及凋亡情况的影响;利用RT-PCR、Real Time PCR和Western blot等方法明确奥曲肽作用于胃癌BGC823细胞后胃泌素基因及蛋白水平的表达变化。[结果]MTT细胞实验显示,奥曲肽对胃癌BGC823细胞的生长和增殖有抑制作用,且存在量效、时效关系和饱和性;流式细胞技术检测结果显示奥曲肽有明显的促进细胞凋亡的作用,使细胞周期阻滞于G1/S期;RT-PCR和Real-time PCR、Western blot结果显示奥曲肽作用于胃癌BGC823细胞后胃泌素的表达变化不明显,蛋白水平表达与基因水平一致。[结论]奥曲肽抑制胃癌增殖可能是通过细胞周期阻滞、诱导细胞凋亡实现的,奥曲肽没有抑制胃泌素表达的作用。     

得斯芬与扶正解毒抗癌复方对肝癌Bel-7402细胞凋亡的对比观察

[目的]对比观察得斯芬与扶正解毒抗癌复方（中药复方）对Bel-7402细胞增殖和凋亡的影响。[方法]2种药物分别作用Bel-7402细胞48h，以EnVision二步法检测细胞Bcl-2、P53蛋白的表达；以流式细胞仪进行凋亡率和细胞周期分析。[结果]50、25μmol／L得斯芬组与10、2mg／ml中药复方组P53表达与对照组比较差异有统计学意义（P〈0．05或〈0．01）；50、25μmol／L得斯芬组与10mg／ml中药复方组在G1峰前出现了明显凋亡峰（Ap峰），凋亡率分别为23．9％、14．7％、5．5％。[结论]得斯芬与扶正解毒抗癌复方可能通过上调P53蛋白的表达、抑制肿瘤细胞DNA合成，使细胞周期停滞在G0／G1期，阻滞细胞进入G2／M期，导致肝癌细胞凋亡。比较结果，得斯芬的抗肝癌效应似乎比扶正解毒抗癌复方更为优越。     

羟基喜树碱诱导胃癌细胞凋亡的实验研究

目的 研究羟基喜树碱(HCPT)诱导胃癌细胞的凋亡作用,探讨其治疗胃癌的作用机制.方法 应用MTT、TUNEL染色、流式细胞仪技术研究HCPT对胃癌细胞SGC-7901、MKN-45、MKN-28的细胞毒和诱导凋亡的作用.结果 HCPT具有很强的细胞毒作用,对三株不同分化程度胃癌细胞的SGC-7901(中分化)、MKN-45(低分化)、MKN-28(6高分化)的IC50为0.008～0.012mg/ml.HCPT作用于细胞后,可看到较为典型的细胞凋亡的形态学变化:细胞核固缩,染色质凝集,呈新月型紧贴于核膜周边,核碎裂,染色质片断化,凋亡小体形成等.流式细胞仪DNA直方图上出现典型的亚二倍体"凋亡峰".流式细胞仪计数显示,HCPT诱导胃癌细胞SGC-7901、MKN-45、MKN-28的凋亡率分别为21.88%、12.35%、30.26%.HCPT诱导胃癌细胞的凋亡率与胃癌的分化程度有关.TDT染色法显示,细胞凋亡指数在12.35%～30.26%之间.HCPT的作用表现为细胞周期特异性,HCPT主要作用于细胞周期的S期,抑制细胞增殖和诱导细胞凋亡,使细胞阻滞于S期.结论 HCPT对胃癌细胞具有很强的细胞毒作用,诱导凋亡是其主要作用机制之一.     

雪松松针总黄酮的体外抗肿瘤作用

目的研究雪松松针总黄酮的体外抗肿瘤活性。方法采用MTT实验进行体外增殖抑制作用研究,从人宫颈癌He La细胞株、人胃癌MKN45细胞株、人肺癌A549细胞株、人肝癌Hep G2细胞株及人胶质瘤SHG44细胞株中筛选雪松松针总黄酮最敏感瘤株,采用细胞流式仪进行细胞周期及凋亡研究。结果雪松松针总黄酮不同浓度对各肿瘤细胞均有增殖抑制作用,并具剂量依赖性,对人肺癌细胞株A549、人肝癌细胞株Hep G2作用48 h后,IC50分别为211.39μg/ml和114.12μg/ml。结合MTT实验结果及IC50值,发现Hep G2细胞对雪松松针总黄酮最为敏感(P<0.05)。雪松松针总黄酮能够阻滞Hep G2细胞于G0/G1期,并诱导其凋亡。结论雪松松针总黄酮不同剂量组对5株肿瘤细胞均有一定抑制作用,其中对Hep G2细胞抑制作用最为显著。     

肼屈嗪对人胃癌细胞株RUNX3基因甲基化及其表达的调节作用

背景:甲基化所致的抑癌基因RUNX3表达沉默是胃癌发生的重要机制,以脱甲基化制剂恢复其表达可起到抗肿瘤作用。目的:研究脱甲基化制剂肼屈嗪对人胃癌细胞株RUNX3基因甲基化及其表达的调节作用,观察肼屈嗪对胃癌细胞生长和凋亡的影响。方法:分别以RT-PCR和甲基化特异性PCR(MSP)检测肼屈嗪和5-Aza-dC处理前后SGC7901、MKN28和MGC803细胞的RUNX3 mRNA表达及其甲基化状态。以MTT法检测MKN28细胞增殖活性,以流式细胞术检测细胞周期和细胞凋亡。结果:MKN28细胞存在甲基化所致的RUNX3基因表达沉默。40μmol/L肼屈嗪作用72 h后,MKN28细胞可扩增出 RUNX3非甲基化条带,呈部分脱甲基化,RUNX3 mRNA恢复表达,但相对表达量低于5-Aza-dC组(P0.05)。10μmol/L以上浓度的肼屈嗪对MKN28细胞生长具有抑制作用,可使细胞周期阻滞于G0/G1期,并诱导细胞凋亡(P0.05)。结论:肼屈嗪可通过脱甲基化恢复RUNX3基因表达并能抑制MKN28细胞生长,诱导细胞凋亡。有必要对肼屈嗪在胃癌治疗中的作用作进一步研究。     

达沙替尼联合奥沙利铂协同抑制胃癌细胞增殖和迁移

目的:评价Src酪氨酸激酶抑制剂达沙替尼联合奥沙利铂抑制胃癌细胞体外增殖、迁移等恶性生物学行为的效应。方法:实时定量-聚合酶链反应(RT-PCR)及蛋白质印迹法(Western blot)检测Src及其活性形式p-Src在胃癌细胞株中的基础表达;蛋白质印迹技术观察不同剂量奥沙利铂作用于胃癌细胞或作用不同时间后,细胞内Src及p-Src的变化规律;细胞计数试剂盒(CCK-8)方法评价胃癌细胞暴露于不同浓度奥沙利铂和达沙替尼后的生长抑制率,分别计算2种药物的半数抑制浓度(IC50),并使用Calcusyn 2.0软件计算联合作用指数(CI);细胞集落形成实验、流式细胞术和划痕实验观察上述药物对胃癌细胞体外增殖、细胞周期、凋亡和迁移能力的影响。结果:胃癌细胞株SGC-7901、BGC-823、MKN-28的p-Src/Src基础表达比值较高;奥沙利铂可明显上调胃癌细胞SGC-7901、BGC-823、MKN-28的p-Src,并呈时间依赖性(r2=0.96、0.85、0.94);达沙替尼和奥沙利铂在胃癌细胞中的CI均     

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.     

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.     

Induction of apoptosis by arsenic trioxide and hydroxy camptothecin in gastriccancer cells in vitro

AIM To study the effects of arsenic trioxide and HCPT on different degrees of differentiated gastric cancer cells (SGC-7901, MKN-45, MKN-28)with respect to both cytotoxicity and induction of apoptosis in vitro. ~ODS The cytotoxicity of As2O3 and HCPT on gastric cancer cells was determined by MTTassay. Morphologic changes of apoptosis of gastric cancer cells were observed by light microscopy and transmission electron microscopy. Apoptosis and cell cycle changes of gastric cancer cells induced by HCPT and As2O3 were investigated by TUNEL method and flow cytometry. RESULTS As2O3 and HCPT had remarkable cytotoxic effects on different degrees of differentiated gastric cancer cells. The IC50 of As2O3 on well differentiated gastric cancer cell MKN-28, moderately differentiated gastric cancer cell SGC-7901, and poorly differentiated gastric cancer cell MKN-28 were 8. 91 μmol/L, 10. 57 μmol/L, and 11.65 μmol/L, respectively. The IC50 of HCPT on MKN-28, SGC-7901, and MKN-45 were 9. 35 rg/L, 10. 21 rg/L, and 12. 63 mg/L respectively after 48 h treatment. After 12 h of exposure to both drugs, gastric cancer cells exhibited morphologic features of apoptosis, including cell shrinkage, nuclear condensation,and formation of apoptotic bodies. A typical subdiploid peak before G0/G1 phase was observed by flow cytometry. The apoptotic rates of SGC7901, MKN-45, and MKN-28 were 13. 84%, 22.52%, and 9. 68%, respectively after 48 h exposure to 10 μmol/L As2O3. The apoptotic rates of SGC-7901, MKN-45, and MKN-28 were 21.88%, 12.35%, and 30. 26%, respectively after 48 h exposure to 10 mg/L HCPT. The apoptotic indice were 7% - 15% as assessed by TUNEL method. The effect of As2O3 on SGC-7901 showed remarkable cell cycle specificity, which induced cell death in G1 phase, and blocked G2/M phase. HCPT also showed a remarkable cell cycle specificity, by inducing cell death and apoptosis in G1 phase and arrest of proliferation at S phase. CONCLUSION AS2O3 and HCPT exhibit significant cytotoxicity on gastric cancer cells by induction of apoptosis. As2O3 and HCPT might have a promising prospect in the treatment of gastric cancer, which needs to be further studied.     

尼美舒利对人胃癌细胞株MKN28细胞周期和PTEN、mTOR基因表达的影响

背景：环氧合酶-2（COX-2）抑制剂的肿瘤化学预防作用已被广泛研究，但其作用机制仍未明确。胛EN为一多肿瘤抑制基因，对mTOR信号途径起负调控作用。目的：探讨选择性COX-2抑制剂尼美舒利对人胃癌细胞株MKN28细胞周期和PTEN、mTOR基因表达的影响。方法：以不同浓度尼美舒利于预MKN28细胞．甲基噻唑基四唑（MYr）实验检测细胞活力，流式细胞分析检测细胞周期，实时荧光定量聚合酶链反应（PCR）检测胛EN、mTORmRNA表达。结果：200～600μmol／L尼美舒利作用24～60h对MKN28细胞增殖有明显抑制作用，且作用呈时间-浓度依赖性。200μmol／L和400μmol／L尼美舒利作用48h可使MKN28细胞周期阻滞于G0／G1期和G2，M期。400pmloFL尼美舒利作用36h和48h可显著上调MKN28细胞PTENmRNA表达，作用24h和36h可显著下调mTORmRNA表达。结论：尼美舒利可通过阻滞细胞周期、调控胛EN、mTOR基因表达抑制人胃癌细胞生长。mTOR信号途径与COX-2通路之间可能存在交互作用。     

5-aza—dC和丁酸钠对人胃癌细胞株MKN28细胞周期、凋亡以及抑癌基因表达的影响

背景：表遗传修饰的主要方式DNA甲基化和组蛋白乙酰化是胃癌发生机制研究中的热点内容。目的：探讨表遗传学调控对人胃癌细胞株MKN28细胞周期、凋广以及抑癌基因Runx3、p21^WAF1表达的影响。方法：培养人胃癌细胞株MKN28,并分为5-氮-2’-脱氧胞苷（5-aza—dC）组、丁酸钠组、5-aza—dC＋丁酸钠组和对照组。以Annexin V—FITC／PI双染法检测细胞周期和凋亡,以逆转录聚合艏链反应（RT—PCR）检测Runx3、p21^WAF1 mRNA表达,以甲基化特异性PCR（MSP）检测Runx3基因启动于区甲基化状态。结果：与对照组相比,5-aza—dC对细胞周期无明显影响,丁酸钠可使细胞周期阻滞于G0／G1期（P〈0．05）;5-aza—dC组和丁酸钠组细胞凋亡率均显著增高（8．3％±1．3％、20．8％±2．4％对2．0％±0．5％,P〈0．05）5-aza—dC可诱导Runx3mRNA重新表达（P〈0．05）,但对p21^WAF1 mRNA表达无影响。丁酸钠可增强p21^WAF1 mRNA表达（P〈0．05）,但不能诱导Runx3 mRNA表达。联合5-aza—dC和丁酸钠可显著绣导细胞凋亡和增强抑癌基因Runx3、p21^WAF1Ⅲ mRNA表达（P〈0．05）．5-azgt—dC十预后,Runx3基因启动子区呈去甲基化状态：结论：去甲基化制剂5-aza-dC或组生白去乙酰化酶抑制剂丁酸钠通过重新表达Runx3或增强p21^WAF1表达而诱导胃癌MKN28细胞凋亡,从而发挥抗肿瘤的作用。     

全反式维甲酸诱导人胃癌细胞凋亡

目的探讨不同分化程度的胃癌细胞凋亡情况和全反式维甲酸对其影响。方法以人胃癌细胞系低分化的ＭＫＮ４５和高分化的ＭＫＮ２８细胞作为研究对象，以不同浓度的全反式维甲酸干预其７２小时后，以原位ＤＮＡ断段切口标记法和ＤＮＡ琼脂糖电泳检测细胞凋亡情况。结果两种细胞系的凋亡率均低于５％，全反式维甲酸干预后凋亡指数上升，且可能与药物浓度有关。结论全反式维甲酸可诱导胃癌细胞凋亡。     

YM155对人胃癌细胞株MKN28的作用及其机制研究

背景:研究发现生存素(survivin)在胃癌组织中高表达,YM155是survivin的特异性抑制剂。目的:探讨YM155对人胃癌细胞株MKN28的作用及其机制。方法:以不同浓度YM155作用于人胃癌细胞株MKN28。采用甲基噻唑基四唑(MTT)法检测细胞增殖抑制率;以原位末端标记(TUNEL法)检测细胞凋亡率;以逆转录聚合酶链反应(RTPCR)、蛋白质印迹法分别检测survivin mRNA和survivin、多聚ADP核糖聚合酶(PARP)、caspase-3蛋白表达。结果:YM155作用后,MKN28细胞增殖抑制,凋亡增加。随着YM155浓度升高,survivin mRNA和蛋白表达水平明显降低,并伴随PARP、caspase-3蛋白裂解。结论:YM155可抑制人胃癌细胞株MKN28增殖,并诱导其凋亡,此机制可能与抑制survivin表达,继而激活caspase凋亡信号通路有关。     

Investigation of the sensitivities of distinct gastric cancer cells to parvovirus H‐1 induced cytotoxicity

OBJECTIVE: To investigate the sensitivities of distinct gastric cancer cells to parvovirus H‐1 induced cytotoxicity and the possible mechanism(s). METHODS: There were six distinct differentiated gastric cancer cell lines: HGC27 (undifferentiated), BGC823 (undifferentiated), MKN45 (poorly differentiated), AGS (poorly differentiated), SGC7901 (moderately differentiated) and MKN28 (well differentiated). The cell cycle distributions were measured by flow cytometry and the differential sensitivities of the six distinct gastric cancer cells after H‐1 virus infection were detected by MTT assay. RT‐PCR was used to detect viral NS1 gene expression in all six gastric cancer cell lines. RESULTS: The S phase ratios of HGC27, BGC823, MKN45, AGS, SGC7901 and MKN28 were 24.72%, 30.15%, 27.10%, 29.03%, 31.82% and 33.73%, respectively. HGC27 cells were sensitive to H‐1 virus induced cytotoxicity, followed by SGC7901 cells. MKN45 and AGS cells were moderately sensitive and MKN28 cells were insensitive. However, BGC823 cells were resistant to H‐1 virus induced cytotoxicity. The expressions of viral NS1 were higher in HGC27, BGC823, MKN45 and SGC7901 cells, and lower in AGS and MKN28 cells. CONCLUSIONS: The sensitivities of the distinct gastric cancer cells to H‐1 virus induced cytotoxicity were markedly different. In general, the poorly differentiated cells showed an enhanced sensitivity to H‐1 virus attack compared with well‐differentiated ones. The enhanced sensitivity of poorly versus well‐differentiated gastric cancer cells to H‐1 virus is related in part to the enhanced capacity of the former for NS1 protein production and accumulation. The undifferentiated BGC823 cells were resistant to H‐1 virus triggered cytotoxicity. It may further verify that not all tumor cells are sensitive to H‐1 virus lytic effects.