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Effect of apoptosis on gastric adenocarcinoma cell line sgc-7901 induced by cis-9,trans-11-conjugated linoleic acid

World Journal of Gastroenterology 2002年第6期8卷 999-1004页

作者： Jia-RenLiu Bing-QingChen Yan-MeiYang Xuan-LingWang Ying-BenXue FoodScienceandToxicology DepartmentofFoodScienceComellUniversityIthacaNY14853-7201USA PublicHealthColleng HarbinMedicalUniversityHarbin150001HeilongjiangProvinceChina

AIM: To determine the effect of apoptosis on gastric cancer cells (sgc-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth.METHODS: Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle,expression of ki67, bcl-2, Fas, and c-myc of sgc-7901 cells which were treated with various c9, t11-CLA concentrations (25,50,100 and 200 μmol@L-1) of c9, t11-CLA for 24h and 48 h,with a negative control (0.1% ethanol).RESULTS: The growth of sgc-7901 cells was inhibited by c9,t11-CLA. Eight days after treatment with various concentrations of c9,t11-CLA, as mentioned above, the inhibition rates were 5.9 %, 20.2 %,75.6 % and 82.4 %, respectively. The frequency of apoptosis on sgc-7901 cells induced by different concentrations of c9, t11-CLA (except for 25 μmol@L-1, 24 h) was significantly greater than that in the negative control (P＜0.01). To further investigate the influence of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of sgc-7901 cells. Immunocytochemical staining demonstrated that sgc-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations for various time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20 %, at 24 h and 8.10-0.20 % at 48 h, respectively), bd-2 (4.30-0.15 % at 24 h and 8.05 %-0 at 48 h),and c-myc(4.85-2.20 % at 24 h and 4.75-0.30 % at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-mycwere 15.1% at 24 h and 13.5 % at 48 h, 6.80 % at 24 h and 8.00 % at 48 h,5.50 % at 24 h and 5.30 % at 48 h, respectively) (P＜0.01),whereas the expressions of Fas were increased (0.60-2.75 %,24 h and 0.45-5.95 %, 48 h).CONCLUSION: The growth and proliferation of sgc-7901 cells are inhibited by cg, t11-CLA via blocking the cell cycle,pathways of bcl-2-associated mito

关键词：胃腺癌细胞系 sgc-7901 亚麻酸衍生物 cis-9 trans-11 诱发凋亡

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Crebanine N-oxide, a natural aporphine alkaloid isolated from Stephania hainanensis, induces apoptosis and autophagy in human gastric cancer sgc-7901 cells

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Asian Pacific Journal of Tropical Biomedicine 2020年第5期10卷 224-231页

作者： Zheng-Wen Wang Hao Liu Geng-Tai Ye Zhi-Yong Sheng Yan-Feng Hu Yin-Feng Tan Guo-Xin Li Department of General Surgery Nanfang HospitalSouthern Medical UniversityGuangzhou 510515GuangdongChina Department of Hepatopancreatobiliary Surgery and General Surgery Hainan Cancer HospitalAffiliated Cancer Hospital of Hainan Medical UniversityHaikou 570312HainanChina Hainan Provincial Key Laboratory of R&D on Tropical Herbs Hainan Medical UniversityHaikou 571199HainanChina

Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in sgc-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and cellular morphology was observed under a microscope. Cell apoptosis was determined by flow cytometry using propidium iodide staining. The expression levels of apoptotic-related proteins, cleaved caspase-3, cytochrome C, p53 and Bax, and autophagyrelated proteins p62, beclin1 and LC3 were detected by Western blotting assays. Results: Crebanine N-oxide treatment significantly inhibited the proliferation of sgc-7901 cells in a dose-dependent and timedependent manner via induction of G2-phase cell cycle arrest, apoptosis, and autophagy in sgc-7901 cells.Conclusions: Crebanine N-oxide could inhibit the growth of gastric cancer cells by promoting apoptosis and autophagy and could be used as a potential agent for treating gastric cancer.

关键词： Crebanine N-oxide Gastric cancer sgc-7901 cells Apoptosis Autophagy

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禾谷镰刀菌胞外多糖诱导sgc-7901细胞凋亡作用及其机制研究

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天然产物研究与开发 2022年第7期34卷 1204-1212页

作者：王姣姣袁平川许寒池陈颖张斯佳田梦云余子琪柳春燕皖南医学院安徽省多糖药物工程技术研究中心皖南医学院药学院药物研发中心活性生物大分子安徽省重点实验室安徽省皖南地区植物药活性筛选与再评价工程实验室芜湖241000

为了探究禾谷镰刀菌胞外多糖(exopolysaccharides from Fusarium graminearum,FGEPS)抗人胃癌细胞sgc-7901作用及其可能的机制,本研究利用液体培养基对禾谷镰刀菌进行发酵培养,通过醇沉、脱色、脱蛋白和透析分离得到胞外多糖,并通过高... 详细信息

为了探究禾谷镰刀菌胞外多糖(exopolysaccharides from Fusarium graminearum,FGEPS)抗人胃癌细胞sgc-7901作用及其可能的机制,本研究利用液体培养基对禾谷镰刀菌进行发酵培养,通过醇沉、脱色、脱蛋白和透析分离得到胞外多糖,并通过高效凝胶渗透色谱、红外光谱和紫外光谱对其进行分析。采用CCK-8法分别检测FGEPS对人胃癌细胞sgc-7901、BGC-823和MGC-803的增殖抑制作用,通过AnnexinV-FITC/PI、Hoechst 33258及JC-1染色分析FGEPS对筛选出的sgc-7901细胞凋亡的影响,进一步通过Western blot法检测促凋亡蛋白Bax、Cleaved Caspase-3、Cleaved Caspase-9和抑凋亡蛋白Bcl-2的表达水平。结果表明从禾谷镰刀菌发酵液中分离出的胞外多糖具有多糖特征吸收峰,不含有多肽核酸类物质,液相色谱显示含有4个多糖组分。CCK-8结果显示FGEPS对sgc-7901细胞的抑制效果最为显著,能显著降低sgc-7901细胞线粒体膜电位,诱导细胞核染色质浓缩,并产生凋亡小体(Psgc-7901细胞中促凋亡蛋白Bax、Cleaved Caspase-3和Cleaved Caspase-9表达(Psgc-7901细胞发生凋亡。

关键词：禾谷镰刀菌胞外多糖 sgc-7901 细胞凋亡线粒体通路

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迷迭香酸对胃癌细胞sgc-7901增殖和凋亡的影响及机制

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中国老年学杂志 2022年第16期42卷 4002-4006页

作者：杨晓南丁玉忠杨桃李雪松褚斌武威市中医医院中医内科甘肃武威733000 武威市中医医院普外科甘肃武威733000 甘肃省肿瘤医院消化肿瘤内一科武威市中医医院胃镜室

目的探讨迷迭香酸(RA)对胃癌细胞sgc-7901生长、增殖、凋亡的影响及机制。方法CCK8检测不同浓度RA对胃癌细胞sgc-7901生长的影响,筛选合适剂量;BrdU检测细胞增殖;流式细胞仪检测细胞凋亡;酶联免疫吸附试验(ELISA)检测氧化应激标志物;荧... 详细信息

目的探讨迷迭香酸(RA)对胃癌细胞sgc-7901生长、增殖、凋亡的影响及机制。方法CCK8检测不同浓度RA对胃癌细胞sgc-7901生长的影响,筛选合适剂量;BrdU检测细胞增殖;流式细胞仪检测细胞凋亡;酶联免疫吸附试验(ELISA)检测氧化应激标志物;荧光探针检测活性氧(ROS);流式检测线粒体膜电位的变化;Western印迹检测线粒体损伤标志物(Bax/Bcl-2、Cleaved cas3/cas3)及Nrf2/HO-1通路(p-Nrf2/Nrf2、NQO1、HO-1)相关蛋白表达。结果与对照组相比,RA浓度为10μmol/L时,RA对细胞生长的抑制作用较小,不具有显著差异。浓度为20μmol/L RA对细胞生长的抑制作用增加,差异显著(Psgc-7901生长、增殖,并促进肿瘤细胞凋亡,显著缓解胃癌的发生发展。

关键词：迷迭香酸胃癌 sgc-7901 凋亡 Nrf2/HO-1通路

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LncRNA-CASC7基因表达下调对胃癌sgc-7901细胞增殖与迁移的影响

LncRNA-CASC7基因表达下调对胃癌SGC-7901细胞增殖与迁移的影响

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作者：韩韬南华大学

学位级别：硕士

目的:通过生物信息学分析CASC7在胃癌中的表达差异,体外细胞实验进一步探索其对胃癌细胞增殖和迁移的影响,为胃癌的诊断与治疗提供理论依据。方法:1.检索De Map、ICGC公共数据库,下载肿瘤样本中CASC7基因表达数据,通过统计学分析,了解CA... 详细信息

目的:通过生物信息学分析CASC7在胃癌中的表达差异,体外细胞实验进一步探索其对胃癌细胞增殖和迁移的影响,为胃癌的诊断与治疗提供理论依据。方法:1.检索De Map、ICGC公共数据库,下载肿瘤样本中CASC7基因表达数据,通过统计学分析,了解CASC7在人体肿瘤中的表达差异以及在胃癌及对应癌旁和正常组织中的表达差异;通过下载并提取GEO、TCGA数据库中与CASC7基因相关的实验数据,统计学分析CASC7在胃癌样本中表达丰度及其与胃癌临床分型之间的关系;通过下载CCLE、De Map数据库胃癌细胞系中CASC7基因的表达数据,统计分析该基因在体外培养胃癌细胞的表达含量,并预测该基因与胃癌细胞生长增殖的相关性,根据结果最后确定敲低该基因最有效的实验方法。2.通过RT-qPCR检测体外培养正常胃粘膜细胞GES-1和胃癌细胞sgc-7901、MGC-803的CASC7基因表达水平是否有差异,选择表达差异最大的细胞作为后续实验对象。3.通过RT-qPCR确定最优结合位点的siRNA,利用瞬时转染技术,沉默CASC7,分别进行CCK-8、平板克隆形成细胞增殖实验和划痕、Transwell细胞迁移实验,对结果进行统计学分析,观察CASC7对实验细胞增殖和迁移能力的影响。结果:1、生信分析显示CACS7在人体肿瘤中有差异表达,在胃癌中高表达,且处于胃癌差异表达Lnc RNA的前列;CASC7在胃癌细胞系中高表达(Psgc-7901、MGC-803中高表达(Psgc-7901表达高于MGC-803;3、CCK-8、平板克隆形成、Transwell和划痕实验显示,下调CASC7基因后,胃癌细胞sgc-7901的增值、迁移能力下降(Psgc-7901中高表达,其表达下调可抑制sgc-7901细胞的增殖和迁移。

关键词： CASC7 sgc-7901 胃癌增殖迁移

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

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World Journal of Gastroenterology 2005年第12期11卷 1829-1832页

作者： LiMa Yong-LeXie YiYu Qiu-NingZhang DepartmentofGastroenterology SecondAffiliatedHospitalLanzhouMedicalUniversityLanzhou730030GansuProvinceChina

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-7901cells.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 MTr 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-2and 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-2and COX-2 gene.

关键词： sgc-7901 丝裂霉素胃肿瘤 Bcl-2 COX-2

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Effects of a Shuangling Fuzheng anticancer preparation on the proliferation of sgc-7901 cells and immune function in a cyclophosphamide-treated murine model

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World Journal of Gastroenterology 2007年第48期13卷 6575-6580页

作者： Hua-Sheng Chen Jue Chen De-Li Cui Yuan-Yuan Zheng Ai-Hua Xu Gang Chen Ling-Chang Jia Yangzhou University Medical College Yangzhou 225001 Jiangsu Province China Jiangsu Province Subei People Hospital Yangzhou 225001 Jiangsu Province China

AIM: To study the inhibitory effects of a Shuangling Fuzheng anticancer preparation (SFAP) on the human gastric cancer cell line sgc-7901 in vitro as well as its immune-modulated effects in a cyclophosphamide-treated murine model. METHODS: MTT experiments and immunocytochemistry ABC experiments were performed for detecting the proliferation of sgc-7901 cells in vitro and protein expression of c-myc. The staphylococcal protein A (SPA) rosette test was utilized for measuring the ratio of T-lymphocyte subsets from peripheral blood in a cyclophosphamide-treated murine model. Enzyme- linked immunosorbant assay (ELISA) was performed for measuring the levels of serum sIL-2R in treated mice, while immunoturbidimetry was used for measuring the levels of immunoglobulins (Ig). RESULTS: SFAP (40-640 mg/L, 48 h) inhibited the proliferation of sgc-7901 cells, and a positive correlation was noted between inhibitory effects and dosage. At a dosage of 160-320 mg/L in cultured cells, the expression of c-myc was decreased. SFAP (50-200 mg/kg) increased the percentage of CD3+ and CD4+ T-lymphocytes, the ratio of CD4/CD8, and the contents of Ig such as IgM, IgG or IgA, but decreased the levels of serum sIL-2R in peripheral blood from cyclophosphamide-treated mice. CONCLUSION: SFAP can inhibit the proliferation of sgc-7901 cells via the c-myc gene. In addition, SFAP can modulat the cellular and humoral immunity in cyclophosphamide-induced immunosuppressed mice.

关键词： sgc-7901 免疫功能细胞增生环磷酰胺抗癌药

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

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World Journal of Gastroenterology 2005年第1期11卷 73-78页

作者： Zhi-GangZhao Wen-LuShen DepartmentofSurgery ShantouUniversityMedicalCollegeShantou515031GuangdongProvinceChina DepartmentofSurgery No.2AffiliatedHospitalShantouUniversityMedicalCollegeShantou515041GuangdongProvinceChina

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 doseand 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 10 μmol/L for 48 h or 8 μmol/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 G1 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

关键词：热休克蛋白70 HSP70 寡核苷酸细胞生长抑制作用细胞凋亡 sgc-7901 胃癌细胞系统

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HSP90抑制剂17-AAG对胃癌sgc-7901细胞生长周期和凋亡的影响

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南方医科大学学报 2013年第2期33卷 271-275页

作者：陈美霓许静洪赵菊梅延安大学医学院实验中心陕西延安716000

目的研究一种特异性的热休克蛋白90抑制剂17-丙烯胺基-17-去甲氧基格尔德霉素(17-AAG)对人胃癌细胞sgc-7901细胞增殖和凋亡的影响,分析其可能的作用机制。方法应用MTT比色法检测不同浓度的17-AAG对胃癌sgc-7901细胞的生长抑制率;荧光显... 详细信息

目的研究一种特异性的热休克蛋白90抑制剂17-丙烯胺基-17-去甲氧基格尔德霉素(17-AAG)对人胃癌细胞sgc-7901细胞增殖和凋亡的影响,分析其可能的作用机制。方法应用MTT比色法检测不同浓度的17-AAG对胃癌sgc-7901细胞的生长抑制率;荧光显微镜下观察PI染色的sgc-7901细胞凋亡形态学变化;采用流式细胞术检测sgc-7901细胞的细胞周期变化及凋亡率变化;通过免疫组化检测胃癌sgc-7901细胞中Fas蛋白的表达。结果 MTT法显示17-AAG能明显抑制胃癌sgc-7901细胞的生长增殖,呈时间、剂量依赖性;流式细胞仪细胞周期分析显示,17-AAG处理48 h后使sgc-7901细胞发生G2/M期阻滞,并有诱导sgc-7901细胞凋亡的作用;细胞免疫组化结果显示,sgc-7901细胞胞浆内有Fas表达,随着药物浓度的加大,阳性表达率也逐渐增加。结论 17-AAG通过改变细胞周期、诱导其凋亡来抑制胃癌sgc-7901细胞的增殖,上调sgc-7901细胞中Fas蛋白的表达是诱导凋亡的作用机制之一。

关键词： 17-AAG 胃癌 sgc-7901 细胞凋亡 Fas蛋白

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幽门螺杆菌刺激胃癌细胞株sgc-7901分泌白细胞介素-8过程中核因子κB的作用

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中华医学杂志 2003年第2期83卷 133-136页

作者：史彤刘文忠高飞萧树东上海第二医科大学附属仁济医院上海市消化疾病研究所 200001 上海第二医科大学细胞生物学教研室

目的　探讨胃上皮细胞在幽门螺杆菌 (Hp)刺激下分泌白细胞介素 8(IL 8)的过程中 ,核因子 κB(NF κB)的作用。方法　电穿孔法将I κBαM(NF κB抑制蛋白 )基因转染入sgc 790 1中 ,β半乳糖苷酶分析转染效率 ,Western印迹分析I κB基因... 详细信息

目的　探讨胃上皮细胞在幽门螺杆菌 (Hp)刺激下分泌白细胞介素 8(IL 8)的过程中 ,核因子 κB(NF κB)的作用。方法　电穿孔法将I κBαM(NF κB抑制蛋白 )基因转染入sgc 790 1中 ,β半乳糖苷酶分析转染效率 ,Western印迹分析I κB基因的表达。将不同浓度的Hp活菌、灭活菌及液体培养上清分别与稳定转染I κB的胃癌细胞株sgc 790 1及其空白质粒对照共同孵育 ,凝胶电泳迁移率变迁分析 (EMSA)和NF κB荧光素酶报告基因分析检测不同时间细胞内NF κB的激活 ,ELISA法检测不同时间细胞上清中IL 8的水平。结果　得到了稳定表达I κB的sgc 790 1细胞 ,命名为sgc790 1 I κB细胞 ,其空白质粒对照命名为sgc790 1 neo。Hp活菌刺激的sgc790 1 neo在 2h和 4h时可检测到明显的NF κB激活 ,灭活菌和液体培养上清刺激下无激活 ;Hp活菌、灭活菌和培养上清刺激下sgc 790 1 I κB内均无NF κB激活。 4h时 ,2× 10 7Hp/ml的Hp活菌刺激下即可检测到sgc790 1 neo内明显的IL 8分泌 ,并有时间剂量依赖效应 ;灭活菌和液体培养上清无此作用。Hp活菌、灭活菌和液体培养上清均不能刺激sgc790 1 I κB产生IL 8。结论　Hp诱导胃上皮细胞分泌IL 8依赖于NF κB的激活。

关键词：幽门螺杆菌胃癌细胞株 sgc-7901 白细胞介素-8 核因子κB

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