曲古抑菌素A对胃癌细胞生长的抑制作用

目的: 研究组蛋白去乙酰化酶抑制剂-曲古抑菌素A(trichostatin A, TSA)对胃癌细胞系SGC-7901的生长抑制作用, 证实该作用是通过促使细胞凋亡而实现的.方法: 用不同浓度(0.2、0.4和0.8 mg/L)和不同作用时间(24、48和72 h)的TSA作用于SGC-7901细胞, 采用MTT法观察TSA对SGC-7901细胞增殖的抑制作用;通过流式细胞仪检测细胞周期和凋亡率的变化;通过透射电镜观察细胞超微结构的变化.结果: TSA可抑制胃癌SGC-7901细胞的生长,且这种作用呈时间和剂量依赖关系. 当TSA作用浓度分别为0.2、0.4和0.8 mg/L时, 与SGC-7901细胞均作用72 h, TSA对SGC-7901细胞生长的抑制率分别为25%±1.2%, 45%±1.4%和73%±1.7%, 各组均与TSA 0.2 mg/L组比较, 差异显著( P<0.05). 当0.8 mg/L TSA分别与SGC-7901细胞作用24、48和72 h, TSA对SGC-7901细胞生长的抑制率分别为21%±1.1%, 37%±2.0%和73%±1.7%, 各组均与TSA作用24 h组比较, 差异显著( P<0.05). TSA可延缓细胞周期, 具有明显的诱导细胞凋亡作用. 电镜下见细胞染色质凝聚成段片状, 细胞核固缩断裂, 核膜破裂, 细胞器及胞膜自溶, 凋亡小体形成.结论: TSA通过诱导细胞周期阻止和凋亡来抑制胃癌细胞系SGC-7901的生长, 且这种作用呈时间和剂量依赖性, 为TSA用于胃癌的治疗提供理论依据.     

Molecule action mechanisms of NM-3 on human gastric cancer SGC-7901 cells in vivo or in vitro

AIM: To study the molecule action mechanisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro. METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg/ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminal deoxynucleotidyl transferase-mediated deoxy-uridine triphosphate-fluorescene nick end labeling (TUNEL) method and flow cytometry analysis. RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smaller than that in normal saline control group (4.17 g+/-0.22 g vs 9.45 g+/-1.38 g, P<0.01). The level of apoptosis of human gastric cell line SGC-7901 was obviously increased in NM-3 treatment group at 1 mg.L(-1) for 24 h. NM-3 inducing apoptotic index in NM-3 plus carboplatin group was 3.5 times that of carboplatin control group (TUNEL: 27.98+/-6.12% vs 12.94+/-2.12%, FACScan: 26.86+/-5.69% vs 11.86+/-1.09%, P<0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg.L(-1). NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer in nude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice. CONCLUSION: NM-3 can inhibit the growth of human gastric cancer cell line SGC-7901, and enhance the sensitivity of carboplatin on SGC-7901 and induced its apoptosis.     

Moleucle action mechunisms of NM-3 on human gastric cancer SGC-7901 Cells in vivo or in vitro

AIM: To study the moleucle action mechunisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro.METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg/ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-fluorescene nick end labeling (TUNEL)method and flow cytometry analysis.RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smaller than that in normal saline control group (4.17 g±0.22 g VS 9.45 g±1.38 g, P＜0.01). The level of apoptosis of human gastric cell line SGC-7901 was obviously increased in NM-3treatment group at 1 mg.L-1 for 24 h. NM-3 inducing apoptotic index in NM-3 plus carboplatin group was 3.5 times that of carboplatin control group (TUNEL: 27.98±6.12 % VS 12.94±2.12 %, FACScan: 26.86±5.69 % VS11.86±1.09 %,P＜0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg.L-L. NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer in nude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice.CONCLUSION: NM-3 can inhibit the growth of human gastric cancer cell line SGC-7901, and enhance the sensitivity of carboplatin on SGC-7901 and induced its apoptosis.     

As2O3与Aspirin联合应用对人胃癌SGC-7901细胞凋亡的影响

目的:观察As2O3与Aspirin联合应用对人胃癌SGC-7901细胞凋亡的影响并探讨其可能机制.方法:As2O3和Aspirin处理SGC-7901细胞,实验分为:阴性对照组、2 mmol/L Aspirin组、1 mmol/L Aspirin组、4 pmoI/L As2O3组、2μmol/L As2O3组和2 Bmol/L As2O3组 1 mmol/LAspirin组,流式细胞术检测As2O3和Aspirin单独及联合应用对SGC-7901细胞凋亡的作用,免疫细胞化学法检测Bcl-2和Bax蛋白的表达.结果:2 μmol/L As2O3 1 mmol/L Aspirin联合应用组与4 μmol/L As2O3组、2 mmol/L Aspirin 组SGC-7901细胞在细胞周期G1期前均出现明显的亚二倍体凋亡峰,差异无明显统计学意义,与阴性对照组细胞、2 μmol/L As2O3及1 mmol/L Aspirin单药组相比,差异均有统计学意义(均P＜0.05).As2O3与Aspirin联合应用组使Bcl-2表达下降,Bax表达增高,与阴性对照组、2 μmol/L As2O3及1 mmol/L Aspirin单药组相比,差异均具统计学意义(50.21%±5.94% VS 91.65%±11.51%,88.66%±10.53%,89.27%±9.84%;40.72%±9.54% VS 21.03%±4.32%,23.07%±6.23%,22.67%±3.1 6%,均P＜0.05).结论:As2O3和Aspirin可能通过改变Bcl-2和Bax表达诱导SGC-7901细胞凋亡,两者联合应用具有协同作用.     

幽门螺杆菌对人胃癌细胞SGC-7901中SHP-2及细胞骨架的影响

目的: 研究幽门螺杆菌(Helicobacterpylori,H pylon)刺激人胃癌细胞SGC-7901后,对细胞内SHP-2表达及细胞骨架的影响.方法: 将临床分离的胃癌Hpylori菌体裂解,以超声提取物刺激SGC-7901细胞1 h,逆转录聚合酶链式反应(RT-PCR)半定量法测定刺激前后SHP-2表达量的变化;并将PCR产物进行克隆和测序.将不同疾病(胃炎,胃溃疡,胃癌)的菌株Hpylori超声提取物刺激SGC-7901细胞10 min,采用phalloidin对细胞内骨架进行荧光染色,研究其对细胞骨架的影响.将野生型和突变型RhoA质粒转入细胞后,再以胃癌Hpylori超声提取物刺激,进一步观察细胞内骨架的变化.结果: 胃癌Hpylori菌体超声提取物刺激SGC-7901细胞1 h后,细胞内SHP-2表达量没有明显变化.胃炎,胃溃疡,胃癌Hpylori菌体超声提取物刺激人胃癌细胞SGC-7901后.与对照组相比,细胞内骨架增多(65.4±0.510,63.37±0.475.64.53±0.522 vs 20.34±1.376.均P<0.05),但这三种菌株间相比无统计学意义.转染入野生型RhoA质粒的细胞经胃癌Hpylori菌体超声提取物刺激后,细胞内骨架较未转染者增多(72.99±1.818vs61.78±1.288,P<0.05),而转染入无活性突变型RhoA质粒的细胞经刺激后,细胞内骨架与未转染者无明显差别.结论: 胃癌Hpylori超声提取物未能引起细胞内SHP-2 mRNA表达量的改变;胃炎,胃溃疡,胃癌Hpylori菌体超声提取物能够增加细胞内骨架的形成,其作用与Hpylori菌种无关,RhoA活性的增强是其中的一个重要中间环节.     

幽门螺杆菌提取物体外对人胃癌细胞SGC-7901形态的影响

目的:探讨幽门螺杆(H pylori)刺激人胃癌细胞SGC-7901后,对细胞形态,迁移以及细胞骨架的影响.方法:从人胃黏膜组织中分离培养H pylori,将得到的H pylori菌体超声裂解,用超声提取物刺激SGC-7901细胞,直接观察SGC-7901细胞形态的变化:细胞迁移活动用Boyden迁移槽和划线法分析;用phalloidin对细胞内F-actin进行荧光染色,研究其对细胞骨架的作用.各组间细胞迁移数量比较用单因素方差分析,组间两两比较用SNK检验:对照组和刺激组细胞发生蜂鸟表型的百分率进行t检验.结果:H pylori菌体超声提取物刺激人胃癌细胞SGC-7901后,细胞的活动性增强,高浓度和低浓度刺激组与对照组相比细胞迁移数明显提高(F=12697.314,P＜0.01),两两之间相比也具有统计学意义(P＜0.01).受刺激后蜂鸟表型细胞数较对照组大大提高(t=29.626,P＜0.01).对照组细胞仅有少量应激纤维形成,H pylori刺激10 min后,应激纤维增加.结论:H pylori可诱导胃癌细胞SGC-7901发生形态改变,促进其迁移,并且增加细胞内细胞骨架的形成.     

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.     

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.     

Apoptosis of human gastric cancer SGC-7901 cells induced by mitomycin combined with sulindac

AIM: To investigate the effects of mitomycin (MMC) combined with sulindac on cell viability, apoptotic induction and expression of apoptosis-related gene Bcl-2 and cyclooxygenase-2 (COX-2) in gastric cancer SGC-7901 cells. METHODS: Human gastric cancer SGC-7901 cells were divided into three treatment groups,namely sulindac treatment group, MMC treatment group and combined sulindac with MMC treatment group. After being treated with drugs, cell viability was examined by MTT assay. Flow cytometry was used to evaluate the cell cycle distribution and apoptotic rates. Morphology of the cells was observed under light microscope and interactive laser microscope. Expression of COX-2 and Bcl-2 was determined by immunocytochemical method. RESULTS: After exposure for 12 h to three kinds of drugs, gastric cancer SGC-7901 cells presented some morphological features of apoptosis, including cell shrinkage, nuclear condensation, DNA fragmentation and formation of apoptotic bodies. Growth inhibition was more obvious in combined sulindac with MMC treatment group and sulindac treatment group than in MMC treatment group. The apoptotic rates in co-treated cells and MMC-treated cells 24 h after treatment were 12.0% and 7.2%, respectively. After exposure for 24 h to MMC, the expression of COX-2 and Bcl-2 protein was up-regulated, COX-2 levels were down-regulated but Bcl-2 gene expression was not changed significantly in combined treatment group. CONCLUSION: MMC-induced apoptosis is reduced by up-regulating the expression of COX-2 and Bcl-2 genes. MMC combined with sulindac can suppress the growth of gastric cancer cells through induction of apoptosis mediated by down-regulation of apoptosis-related Bcl-2 and COX-2 gene.     

罗格列酮对人胃癌细胞系迁移侵袭的抑制及其机制

目的:探讨罗格列酮对人胃癌SGC7901、SGC7901/VCR细胞侵袭转移能力及LIMK1基因蛋白表达的影响.方法:罗格列酮(40 mg/L)作用SGC7901和SGC7901/VCR细胞24 h后,采用划痕实验和Transwell实验分别观察罗格列酮对细胞的迁移和侵袭能力.RT-PCR检测LIMKl mRNA和co...     

葡萄糖神经酰胺合成酶基因在人胃癌细胞SGC-7901及SGC-7901/VCR的表达和意义

目的:研究葡萄糖神经酰胺合成酶(glucosyl- ceramide synthase,GCS)基因在人胃癌细胞SGC-7901和SGC-7901/VCR的表达并探讨其对人胃癌发生、发展的意义.方法:体外培养人亲本敏感胃癌细胞SGC-7901和人耐长春新碱胃癌细胞SGC-7901/VCR.采用MTT法检测半数细胞抑制浓度(IC_(50))和SGC-7901/VCR耐药倍数;RT- PCR法检测SGC-7901和SGC-7901/VCR两种细胞GCS mRNA的表达,免疫组化法测定GCS蛋白表达水平.结果:SGC-7901和SGC-7901/VCR的IC_(50)分别为1.40±0.06和86.20±0.50 mg/L.SGC-7091/ VCR细胞耐药指数是亲本细胞SGC-7901的61倍,SGC-7901和SGC-7901/VCR两种细胞均有GCS mRNA表达,且SGC-7901/VCR细胞GCS mRNA表达水平(GCS指数为3.9)较SGC-7901细胞(GCS指数为0.5)有显著升高(P<0.05),耐药细胞GCS蛋白表达阳性率(65%)显著高于亲本细胞(18%)(P<0.05).结论:GCS基因在人胃癌耐药细胞和亲本敏感细胞均有表达,耐药细胞GCS mRNA及蛋白均高表达.GCS可能参与了胃癌的发生过程,且与肿瘤多药耐药有密切关系.     

RRR—α—tocopheryl succinate inhibits human gastr cancer SGC—7901 cell growth by inducing apoptos and DNA synthesis arrest

AIM: To investigate the effects of growth inhibition of human gastric cancer SGC-7901 cell with RRR-alpha-tocopheryl succinate (VES), a derivative of natural Vitamin E, via inducing apoptosis and DNA synthesis arrest. METHODS: Human gastric cancer SGC-7901 cells were regularly incubated in the presence of VES at 5, 10 and 20mg x L(-1) (VES was dissolved in absolute ethanol and diluted in RPMI 1640 complete condition media correspondingly to a final concentration of VES and 1 mL x L(-1) ethanol), succinic acid and ethanol equivalents as vehicle (VEH) control and condition media only as untreated (UT) control. Trypan blue dye exclusion analysis and MTT assay were applied to detect the cell proliferation. Cells were pulsed with 37kBq of tritiated thymidine and (3H) TdR uptake was measured to observe DNA synthesis. Apoptotic morphology was observed by electron microscopy and DAPI staining. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect VES-triggered apoptosis.RESULTS: VES inhibited SGC-7901 cell growth in a dose-dependent manner. The growth curve showed suppression by 24.7%, 49.2% and 68.7% following 24h of VES treatment at 5, 10 and 20 mg x L(-1), respectively, similar to the findings from MTT assay. DNA synthesis was evidently reduced by 35%, 45% and 98% after 24h VES treatment at 20mg x L(-1) and 48 h at 10 and 20mg x L(-1), respectively. VES induced SGC-7901 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation/margination, nucleus fragmentation and apoptotic body formation, typical apoptotic sub-G1 peak by flow cytometry and increase of apoptotic cells by TUNEL assay in which 90% of cells underwent apoptosis after 48 h of VES treatment at 20 mg x L(-1). CONCLUSION: VES can inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesis arrest. Inhibition of SGC-7901 cell growth by VES is dose- and time-dependent. Therefore VES can function as a potent chemotherapeutic agent against human gastric carcinogenesis.     

Roles of Fas signaling pathway in vitamin E succinateinduced apoptosis in human gastric cancer SGC—7901 cells

AIM: To investigate the roles of Fas signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS: Human gastric cancer SGC-7901 cells were treated with VES at 5, 10, 20 mg x L(-1), succinic acid and vitamin E as vehicle control and condition media only as untreated (UT) control. Apoptotic morphology was observed by DAPI staining. Western blot analysis was applied to measure the expression of Fas, FADD and caspase-8 proteins. After the cells were transiently transfected with Fas and FADD antisense oligonucleotides, respectively, caspase-8 activity was determined by flurometric method. RESULTS: The morphologically apoptotic changes were observed after VES treatment by DAPI staining. 23.7 % and 89.6 % apoptosis occurred after 24 h and 48 h of 20 mg x L(-1) VES treatment, respectively. The protein levels of Fas, FADD and caspase-8 were evidently increased in a dose-dependent manner after 24 h of VES treatment. The blockage of Fas by transfection with Fas antisense oligonucleotides obviously inhibited the expression of FADD protein. After SGC-7901 cells were transfected with Fas and FADD antisense oligonucleotides, caspase-8 activity was obviously decreased (P<0.01), whereas Fas blocked more than FADD. CONCLUSION: VES-induced apoptosis in human gastric cancer SGC-7901 cells involves Fas signaling pathway including the interaction of Fas, FADD and caspase-8.     

MUC2反义脱氧寡核苷酸对胃癌细胞体外黏附侵袭活性的影响

目的 探讨黏蛋白MUC2反义脱氧寡核苷酸（ASODN）对人胃癌细胞株SGC7901黏附侵袭活性的影响。方法 采用人工合成的MUC2 ASODN经阳离子脂质体包裹后转染入SGC7901细胞中,采用黏附试验、Boyden小室体外侵袭试验观察比较转染前后癌细胞黏附率,穿膜细胞相对百分率及组织蛋白酶D、钙黏蛋白表达的变化。结果 转染SGC7901细胞48h后,癌细胞黏附率在30、60、90、120min各时间段逐渐升高,但低于空白对照组（P均〈0．01）;转染后癌细胞穿膜细胞相对百分率明显下降;转染后SGC7901细胞的E-钙黏蛋白表达明显增高,组织蛋白酶D水平明显降低。结论 人工合成的MUC2 ASODN能有效抑制胃癌细胞株SGC7901黏附侵袭能力。     

Paris chinensis dioscin induces G2/M cell cycle arrest and apoptosis in human gastric cancer SGC-7901 cells

AIM:To investigate the anti-tumor effects of Paris chinensis dioscin(PCD)and mechanisms regarding cell cycle regulation and apoptosis in human gastric cancer SGC-7901 cells.METHODS:Cell viability was analyzed by the 3-(4,5-di-methylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay.Cell apoptosis was evaluated by flow cytometry and laser scanning confocal microscope(LSCM)using Annexin-V/propidium iodide(PI)staining,and the cell cycle was evaluated using PI staining with flow cytom-etry.Intracellular calci...     

Heat shock protein 70 antisense oligonucleotide inhibits cell growth and induces apoptosis in human gastric cancer cell line SGC-7901

AIM: Heat shock protein (HSP)70 is over-expressed in human gastric cancer and plays an important role in the progression of this cancer. We investigated the effects of antisense HSP70 oligomer on human gastric cancer cell line SGC-7901, and its potential role in gene therapy for this cancer. METHODS: Human gastric cancer cell line SGC-7901 was treated in vitro with various concentrations of antisense HSP70 oligonucleotides at different intervals. Growth inhibition was determined as percentage by trypan blue dye exclusion test. Extracted DNA was electrophoresed on agarose gel, and distribution of cell cycle and kinetics of apoptosis induction were analyzed by propidium iodide DNA incorporation using flow cytometry, which was also used to detect the effects of antisense oligomer pretreatment on the subsequent apoptosis induced by heat shock in SGC-7901 cells. Proteins were extracted for simultaneous measurement of HSP70 expression level by SDS-PAGE Western blotting. RESULTS: The number of viable cells decreased in a dose-and time-dependent manner, and ladder-like patterns of DNA fragments were observed in SGC-7901 cells treated with antisense HSP70 oligomers at a concentration of 10μmol/L for 48 h or 8μmol/L for 72 h, which were consistent with inter-nucleosomal DNA fragmentation. Flow cytometric analysis showed a dose- and time-dependent increase in apoptotic rate by HSP70 antisense oligomers. This response was accompanied with a decrease in the percentage of cells in the G_1 and S phases of the cell cycle, suggesting inhibition of cell proliferation. In addition, flow cytometry also showed that pretreatment of SGC-7901 cells with HSP70 antisense oligomers enhanced the subsequent apoptosis induced by heat shock treatment. Western blotting demonstrated that HSP70 antisense oligomers inhibited HSP70 expression, which preceded apoptosis, and HSP70 was undetectable at the concentration of 10 μmol/L for 48 h or 8 μmol/L for 72 h. CONCLUSION: Antisense HSP70 oligomers can abrogate HSP70 expression in SGC-7901 cells, which may in turn induce apoptosis and inhibit cell proliferation, conversely suggesting that HSP70 is required for the proliferation and survival of human gastric cancer cells under normal conditions.     

奥曲肽对人胃癌SGC-7901裸鼠种植瘤生长的影响

目的观察生长抑素类似物奥曲肽在体内对胃癌生长的影响。方法人胃癌细胞株SGC7901细胞接种于48只裸鼠背部皮下制成荷瘤动物模型。第8天将裸鼠随机分成4组:奥曲肽(Oct组,100μg/kg;s.c.qd);5Fu组(17mg/kg,ip,2次/周);奥曲肽和5Fu联合治疗组(联合治疗组);对照组,每组各12只裸鼠。连续用药6周。末次用药24小时后处死动物,检测肿瘤体积、重量、坏死体积,比较抑瘤率。结果奥曲肽组、5Fu组、联合治疗组、对照组的平均瘤体体积(cm3)分别为2.17±0.78、2.19±0.79、1.36±0.75、3.23±0.74(F=9.317,P=0.0001);平均瘤体重量(g)分别为6.88±2.06、7.22±2.47、4.47±2.28、10.30±2.80(F=5.452,P=0.0001);平均坏死体积(cm3)分别为0.55±0.38、0.52±0.53、1.14±0.83、0.32±0.27(F=13.987,P=0.0001);奥曲肽组、5Fu组、联合治疗组的抑瘤率分别为:33.20%、29.92%、56.60%(χ2=6.461,P=0.04)。结论奥曲肽可以抑制裸鼠胃癌移植瘤的生长。