芫菁斑蝥素对喉癌细胞和胃癌细胞的抑制作用

【目的】 研究提取自眼斑芫菁Mylabris cichorii (Linnaeus)体内的斑蝥素对人喉癌HEP-2细胞和人胃癌BGC-823细胞的抑制、以及对细胞周期分布的影响。【方法】 将斑蝥素作用于经体外培养的人喉癌HEP-2细胞和人胃癌BGC-823细胞, 采用MTT法进行体外细胞抑制实验, 测定斑蝥素对这2种癌细胞生长的抑制率与剂量效应;采用流式细胞术测定斑蝥素处理的人喉癌HEP-2细胞的细胞周期;并通过光学显微镜观察其细胞形态学改变。【结果】 斑蝥素浓度为1.28 μmol/L时, 对HEP-2细胞有显著抑制作用, 且随药物浓度升高其抑制作用增强, 呈剂量效应关系, 抑制中浓度为2.88 μmol/L;斑蝥素浓度为20.4 μmol/L时, 对BGC-823细胞有显著抑制作用, 且随药物浓度升高其抑制作用增强, 呈剂量效应关系, 抑制中浓度为54.85 μmol/L。用浓度1.44和2.88 μmol/L的斑蝥素处理HEP-2细胞24 h后, G2-M期分布从8.21%增加到22.29%, S期细胞分布从14.33%增加到21.61%, 且随药物浓度升高其阻滞作用增加, 呈剂量效应关系。G0-G1期细胞分布都有所降低, 从77.45%降低到56.10%, G0-G1期峰前无显著的亚二倍体峰出现, 说明斑蝥素未能够诱导HEP-2细胞发生凋亡。光镜检查显示：HEP-2细胞可出现细胞收缩、胞膜突出、核碎裂等现象。【结论】 斑蝥素对治疗喉癌的效果可能较为理想, 而对胃癌的作用则不明显。     

Tetrandrine Induces Mitochondria-Mediated Apoptosis in Human Gastric Cancer BGC-823 Cells

Tetrandrine, a bis-benzylisoquinoline alkaloid isolated from the dried root of Hang-Fang-Chi ( Stephania tetrandra S. Moore), has been reported to possess anti-cancer effects on many tumors. In this study, we investigated tetrandrine-induced apoptosis on human gastric cancer BGC-823 cells in vitro and in vivo. The results showed that tetrandrine significantly inhibited cell viability in a dose- and time-dependent manner and induced apoptosis. It increased the apoptosis; upregulation of Bax, Bak, and Bad; and downregulation of Bcl-2 and Bcl-xl in BGC-823 cells. Moreover, tetrandrine increased the activation of caspase-3 and -9, release of cytochrome c, and upregulation of apaf-1, suggesting that tetrandrine-induced apoptosis was related to the mitochondrial pathway. Meanwhile, pretreatment with the pan-caspase inhibitor z-VAD-fmk in BGC-823 cells reduced tetrandrine-induced apoptosis by blocking activation of caspases. Furthermore, tetrandrine effectively inhibited tumor growth via apoptosis induction, which was verified by immunohistochemical analysis in a nude mouse xenograft model. Taken together, we concluded that tetrandrine significantly inhibited the proliferation of gastric cancer BGC-823 cells through mitochondria-dependent apoptosis, which may play a promising role in gastric cancer therapy.     

RASAL1 influences the proliferation and invasion of gastric cancer cells by regulating the RAS/ERK signaling pathway

The aim of this study was to investigate the biological characteristics of the RASAL1 gene in a well-differentiated gastric cancer cell line MKN-28 and a poorly differentiated gastric cancer cell line BGC-823 cells, using RNA interference and gene transfection technology, respectively. MKN-28 cells were transfected with the shRNA of RASAL1 and BGC-823 cells were transfected with the pcDNA 3.1 plasmid vector containing RASAL1. RT-PCR and western blotting were then used to detect the expression of RASAL1 mRNA and protein. The activities of RAS and extracellular signal-regulated kinase 1/2 were analyzed by the pull-down method and western blotting. The proliferate capacity, apoptosis rate, invasive and migratory potentials of MKN-28 or BGC-823 cells were also measured by Cell Counting Kit-8 cell proliferation assay, propidium iodide/Annexin V staining coupled with flow cytometry, and transwell chamber assays, respectively. Measurement of RASAL1 mRNA and protein expression in two cells revealed successful transfection of the shRNA of RASAL1 and RASAL1-pcDNA3.1 plasmid into these two cells. Moreover, decreased expression of RASAL1 in MKN-28 cells resulted in increased expression of RAS-GTP and p-ERK1/2. Interestingly, decreased expression of RASAL1 inhibited apoptosis and facilitated cell proliferation, invasion and migration. The increased expression of RASAL1 in BGC-823 cells caused declined expression of RAS-GTP and p-ERK1/2, as well as promoted apoptosis and restrained cell proliferation, invasion and migration. The down-regulation of RASAL1 promoted the proliferation, invasion and migration of gastric cancer MKN-28 cells, and up-regulation of RASAL1 inhibited the proliferation, invasion and migration of BGC-823 gastric cancer cells by regulating the RAS/ERK signaling pathway. Thus, our results suggest that RASAL1 may play an important role as a tumor suppressor gene in gastric cancer.     

蛹虫草对人胃癌细胞BGC-823生长抑制与诱导凋亡作用研究

目的研究蛹虫草水提物（the aqueous extract of Cordycep Militaris,AEoCM）对人胃癌细胞（BGC-823）生长抑制与凋亡诱导作用。方法采用不同浓度的AEoCM分别作用于胃癌BGC-823细胞,24、48和72h后,应用倒置相差显微镜观察胃癌细胞的形态变化,四氮甲基唑蓝（MTT）测定细胞生长抑制效应,流式细胞仪（FCM）检测细胞周期变化及凋亡率,免疫组化方法测定NK-k BP65的表达。结果AEoCM能显著抑制BGC-823细胞增殖,且在一定的浓度范围内呈时问和浓度依赖性。形态学观察发现,细胞变暗、皱缩,形状不规则;FCM检测结果显示,G2期的细胞于作用72h后分布显著增加,使细胞阻滞于G2期。0．5g／L AEoCM在24、48和72h凋亡率分别为4．655％、11．039％和19．368％,其凋亡程度与时间呈正相关,免疫组化方法测定NK-k BP65的表达下调。结论AEoCM能明显抑制BGC-823细胞的生长,诱导其细胞凋亡,其诱导细胞凋亡的机制可能与下调NK—k BP65的表达有关。     

人胃癌细胞株裸鼠皮下移植瘤模型的建立及其生物学特性

目的初步建立不同浓度下制备人胃癌细胞株BGC-823裸鼠皮下移植瘤模型,观察其生物学特性。方法培养人胃癌细胞系BGC-823细胞,并分别以四个浓度皮下注射于裸鼠腋下每只0.2 mL。根据BGC-823细胞注射浓度将40只裸鼠随机分为四组：组一5×107个活细胞/mL（n=10）;组二1×107个活细胞/mL（n=10）;组三1×106个活细胞/mL（n=10）;组四1×105个活细胞/mL（n=10）。观察各组裸鼠摄食、活动情况、精神状态、死亡率、成瘤时间、成瘤率、肿瘤生长情况,采用免疫组化法检测肿瘤微血管密度。结果各组裸鼠摄食、精神情况正常,无死亡现象。除组四1×105个活细胞/mL浓度组成瘤率为0%外,其余各组成瘤率均为100%,瘤体出现时间在3～7 d,肿瘤血管密度MVD平均为：（123.26±31.57）个/mm2。结论初步建立了人胃癌裸鼠皮下移植瘤模型及建立此细胞系模型的最低浓度。为胃癌的进一步研究奠定了基础。     

Dihydroartemisinin induces apoptosis in human gastric cancer cell line BGC-823 through activation of JNK1/2 and p38 MAPK signaling pathways

Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, is associated with a broad range of biological properties including antitumor activity. However, the effect of DHA on gastric cancer has not been clearly clarified. The aim of this study was to investigate the role and mechanism of DHA in human gastric cancer cell line BGC-823. Cell viability was assessed by MTT assay. Cell apoptosis was analyzed with flow cytometry. The expressions of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38 MAPK) and their phosphorylated forms as well as apoptosis related proteins were examined by western blot analysis. The results demonstrated that DHA inhibited cell viability of BGC-823 cells in a dose- and time-dependent manner. DHA treatment upregulated the expression of Bax, cleaved caspase-3 and -9, and degraded form of PARP, and downregulated the Bcl-2 expression and Bcl-2/Bax ratio. Meanwhile, DHA increased the phosphorylation of ERK1/2, JNK1/2 and p38 MAPK. Synthetic inhibitors of JNK1/2 or p38 MAPK kinase activity, but not inhibitor of ERK1/2, significantly abolished the DHA-induced activation of caspase-3 and -9. In vivo tumor-suppression assay further indicated that DHA displayed significant inhibitory effect on BGC-823 xenografts in tumor growth. These results indicate that DHA induces apoptosis of BGC-823 cells through JNK1/2 and p38 MAPK signaling pathways and DHA could serve as a potential additional chemotherapeutic agent for treatment of gastric cancer.     

Sprouty-2对胃癌细胞上皮间质转化及侵袭转移的影响

目的:研究Sprouty2(SPRY2)基因在胃癌肿瘤细胞上皮间质转化(EMT)和侵袭转移的影响。方法:体外培养人胃癌细胞(BGC-823),采用慢病毒介导的sh RNA沉默SPRY2基因,并用实时定量PCR与Western blot检测其SPRY2、E-钙黏蛋白(E-cadherin)、波形蛋白(vimentin)的表达,采用细胞划痕实验、Transwell实验检测SPRY2基因沉默后的胃癌细胞侵袭转移能力变化。结果:在慢病毒介导sh RNA沉默SPRY2基因的人胃癌BGC-823细胞中,SPRY2的m RNA和蛋白表达明显降低(P0.05),SPRY2沉默后人胃癌细胞E-cadherin的蛋白表达增多(P0.05),vimentin的蛋白表达减少(P0.05)。此外,SPRY2沉默后,胃癌细胞迁移能力和侵袭能力明显减弱(P值均P0.05)。结论:Sprouty-2基因通过调节E-cadherin与vimentin的表达参与胃癌细胞的上皮-间质转化,进而促进胃癌细胞的迁移与侵袭。     

CDX2基因高表达对胃癌细胞生物学行为的影响

目的探讨尾侧型同源转录因子-2(CDX2)基因过表达对胃癌BGC-823细胞增殖、迁移、凋亡等生物学特征的影响。方法采用脂质体转染法建立CDX2基因过表达的胃癌BGC-823稳定细胞株,分别采用RT-PCR、Western blotting和免疫细胞化学等方法检测转染重组表达载体pEGFP-C1/CDX2后,BGC-823细胞中CDX2基因及其蛋白的表达。MTT法检测CDX2基因过表达对细胞的增殖能力的影响;划痕实验检测CDX2过表达对细胞迁移能力的影响;流式细胞术检测CDX2过表达对细胞的凋亡的影响;应用基因芯片技术检测转染前后相关基因的差异表达。结果 RT-PCR及Western blotting检测结果显示,与对照组相比,转染pEGFP-C1/CDX2后,BGC-823细胞中CDX2基因和蛋白均呈高表达;CDX2过表达能明显降低转然组BGC-823细胞增殖能力和迁移能力;但对细胞凋亡影响不明显;基因芯片结果提示CDX2基因高表达能影响某些基因的表达。结论 CDX2过表达能明显抑制胃癌细胞增殖、降低迁移能力,提示CDX2在胃癌中可能发挥抑癌基因的作用。     

CARP Is a Potential Tumor Suppressor in Gastric Carcinoma and a Single-Nucleotide Polymorphism in CARP Gene Might Increase the Risk of Gastric Carcinoma

Background

The caspase-associated recruitment domain-containing protein (CARP) is expressed in almost all tissues. Recently, the tumor-suppressive function of CARP was discovered and attracted increasing attention. This study aimed to investigate the role of CARP in the carcinogenesis of human gastric carcinoma.

Methodology/Principal Findings

Compared with normal gastric tissue, the downregulation of CARP expression was observed in gastric carcinoma tissue by cDNA array and tissue microarray assay. In vitro, the gastric carcinoma cell line (BGC-823) was stably transfected with pcDNA3.1B-CARP or plus CARP siRNA, and we used MTT, flow cytometry, cell migration on type I collagen, cell-matrix adhesion assay and western blot analysis to investigate the potential anti-tumor effects of CARP. The data showed that overexpressing CARP suppressed the malignancy of gastric carcinoma BGC-823 cell line, including significant increases in apoptosis, as well as obvious decreases in cell proliferation, migration, adhesion ability, and tumor growth. The tumor-suppressive effects of CARP were almost restored by siRNA-directed CARP silence. In addition, overexpression of CARP induced G1 arrest, decreased the expressions of cyclin E and CDK2, and increased the expressions of p27, p53 and p21. In vivo, the tumor-suppressive effect of CARP was also verified. A single-nucleotide polymorphism (SNP) genotype of CARP (rs2297882) was located in the Kozak sequence of the CARP gene. The reporter gene assay showed that rs2297882 TT caused an obvious downregulation of activity of CARP gene promoter in BGC-823 cells. Furthermore, the association between rs2297882 and human gastric carcinoma susceptibility was analyzed in 352 cases and 889 controls. It displayed that the TT genotype of rs2297882 in the CARP gene was associated with an increased risk of gastric carcinoma.

Conclusions/Significance

CARP is a potential tumor suppressor of gastric carcinoma and the rs2297882 C>T phenotype of CARP may serve as a predictor of gastric carcinoma.     

Inhibition of two gastric cancer cell lines induced by fucoxanthin involves downregulation of Mcl-1 and STAT3

Fucoxanthin is a natural carotenoid that had never been previously demonstrated to have anti-tumor effect on human gastric adenocarcinoma SGC-7901 or BGC-823 cells. Here it was found to inhibit proliferation and induce apoptosis through JAK/STAT signal pathway in these cells; the mechanism by which this occurred was investigated. We find that fucoxanthin significantly increased the number of apoptotic cells by propidium iodide (PI) dye staining and flow cytometry. Fucoxanthin (50 or 75 μM) induced SGC-7901 cells cycle arrest at S phase, while BGC-823 cells arrest at G2/M phase. RT-PCR and western blot analysis revealed that the expressions of Mcl-1, STAT3 and p-STAT3 were obviously decreased by fucoxanthin in a dose-dependent manner. Synthetic siRNA targeting Mcl-1 was transfected into cells which had no effect on expressions of STAT3. After pretreatment with AG490 (50 μM) which led to blocking of the JAK/STAT signal pathway, the reductive expressions of Mcl-1, STAT3 and p-STAT3 caused by fucoxanthin were inhibited. This is the first analysis of effects on SGC-7901 and BGC-823 cells by fucoxanthin. Fucoxanthin can induce cell-cycle arrest and apoptosis in these cells. These effects involved downregulation of Mcl-1, STAT3 and p-STAT3. This work is significant for better understanding of mechanisms leading to human gastric adenocarcinoma formation and informing exploitation of anti-tumor marine drug, and for providing Mcl-1 and STAT3 as potential therapeutic targets for gastric adenocarcinoma.     

大豆低聚糖对人胃癌细胞株BGC-823细胞的细胞凋亡和细胞周期的影响

目的通过观察大豆低聚糖对胃癌癌细胞株BGC-823细胞的细胞周期和细胞凋亡的影响,探索乳酸杆菌发酵滤液对胃癌细胞作用的可能机制。方法用光镜和流式细胞仪分析不同浓度大豆低聚糖对BGC-823细胞的凋亡诱导效果;用流式细胞仪分析不同浓度大豆低聚糖对BGC-823细胞细胞周期的影响。结果大豆低聚糖可以诱导BGC-823细胞的凋亡。形态学观察处理后的BGC-823细胞,可见细胞变形,细胞皱缩,体积变小,细胞间隙增大,细胞核固缩。流式细胞仪分析50 mg/ml和100 mg/ml大豆低聚糖作用48 h和72 h BGC-823细胞的凋亡比例,分别为6.76%和7.93%。50 mg/ml大豆低聚糖作用48 h,引起BGC-823细胞G1期阻滞,100 mg/ml大豆低聚糖作用48 h,引起BGC-823细胞出现S期阻滞。结论大豆低聚糖可诱导部分BGC-823细胞凋亡。大豆低聚糖对BGC-823细胞的生长抑制作用在低浓度时可能通过G1期阻滞实现,在高浓度时可能通过S期阻滞实现。     

转录因子SOX2 对胃癌干细胞自我更新、增殖和迁移的影响

目的:检测SOX2在胃癌组织中的表达,探讨SOX2对胃癌干细胞自我更新、增殖和转移能力的影响。方法:采用免疫组化检测SOX2在胃癌及癌旁组织中的表达情况。通过肿瘤球形成实验富集、分离胃癌干细胞。构建SOX2过表达慢病毒并感染胃癌干细胞中,通过实时定量PCR和western bolt检测感染慢病毒后胃癌干细胞中SOX2表达情况。分别利用肿瘤球形成实验检测SOX2对胃癌肿瘤干细胞自我更新能力的影响,CCK-8实验检测SOX2对胃癌干细胞增殖能力的影响,流式细胞术分析SOX2对胃癌干细胞的细胞周期的影响,Transwell实验检测SOX2对胃癌干细胞转移能力的影响。结果:SOX2在胃癌组织中表达显著低于癌旁组织。肿瘤球形成实验能够有效富集胃癌细胞SGC-7901和BGC-823的干细胞。慢病毒载体感染能够显著增强SOX2在胃癌干细胞中的表达。过表达SOX2能够抑制胃癌干细胞的自我更新、增殖和侵袭能力。结论:SOX2在胃癌中发挥抑癌基因的功能,其机制可能通过抑制肿瘤干细胞的自我更新、增殖和侵袭转移能力而抑制胃癌的发生发展。     

红车轴草提取物对胃癌BGC-823细胞凋亡的影响

探讨红车轴草(TrifoliumpratenseL)提取物对胃癌细胞株BGC-823的抑制增殖效应及诱导凋亡作用.我们采用不同浓度(50、100、250、500、1000mg/L)红车轴草提取物处理BGC-823细胞,采用四甲基偶氮唑盐(MTT)法检测药物对细胞的抑制作用,倒置显微镜观察细胞的形态学改变;AO/EB染色,荧光显微镜观察细胞凋亡形态;采用DNALadder观察DNA的降解;应用流式细胞仪观察细胞凋亡过程中的细胞周期的变化和细胞凋亡.结果显示在红车轴草提取物的作用下,BGC-823细胞呈凋亡改变,DNA琼脂糖凝胶电泳呈典型的凋亡特征.细胞凋亡的同时,细胞周期阻滞于G2/M期.实验结果表明红车轴草提取物能抑制胃癌BGC-823细胞增殖,能诱导胃癌细胞凋亡.     

毛喉萜对人胃癌细胞BGC－823中蛋白激酶C及其亚类的影响

以人胃癌细胞ＢＧＣ－８２３为模型,研究了毛喉萜（ｆｏｒｓｋｏｌｉｎ）对胃癌细胞中蛋白激酶Ｃ活性及其亚类基因表达的作用,同时也观察了毛喉萜对癌基因ｃ－ｊｕｎ及抑癌基因ｐ５３表达的影响．结果表明,２×１０~（－５）ｍｏｌ／Ｌ毛喉萜处理ＢＧＣ－８２３细胞７２ｈ,细胞质、膜和细胞核ＰＫＣ活性下降,ＰＫＣ亚类β,γ基因表达被抑制,癌基因ｃ－ｊｕｎ的表达也明显降低,而抑癌基因ｐ５３表达升高,上述变化可能是毛喉萜抑制胃癌细胞增殖等生理效应的重要分子事件。     

Retracted: Curcumin derivative L6H4 inhibits proliferation and invasion of gastric cancer cell line BGC-823

Curcumin and its chalcone derivatives have well-known, explicit biological antitumor properties, such as instance antiproliferative and apoptotic effects via multiple molecular targets. In this study, we investigated the anticancer activity of curcumin derivative L6H4 (curcumin L6H4) on gastric cancer cells. Inhibitory effects of curcumin L6H4 on gastric cancer cells (BGC-823) were studied by the diphenyltetrazolium (MTT) assay, and cell apoptosis was detected by Annexin-V/propidium iodide (PI) staining and then analyzed by flow cytometry. A mouse xenotransplant gastric tumor model was established to detect the role of curcumin L6H4 in vivo. The apoptosis-related proteins p53, p21, Bax, and Bcl-2 in BGC-823 cells and mouse xenotransplant models treated with curcumin L6H4 were determined by Western blot analysis. Curcumin L6H4 can significantly inhibit the proliferation and induce the apoptosis of BGC-823 cells, thus enhancing the expression levels of p53, p21, Bax, and Bcl-2 noticeably in vivo and in vitro. Meanwhile, curcumin L6H4 can remarkably suppress the growth of tumor cells in animal models. These results suggest that curcumin derivative L6H4 has potent of antitumor properties in vitro or in vivo.     

Synthesis of [3β-acetoxy-urs-12-en-28-oyl]-1-monoglyceride and investigation on its anti tumor effects against BGC-823

Ursolic acid (UA) as the leader compound was designed to prepare a series of derivatives (three novel compounds UA-1a, UA-1b and UA-2) by modification at the C3 and C28 positions. Their chemical structures were confirmed by IR, (1)H NMR and MS. The cytotoxic activity of the derivatives was evaluated against HepG2, BGC-823 and HT-29 by the MTT assay. The novel derivative UA-1a, [3β-acetoxy-urs-12-en-28-oyl]-1-monoglyceride showed significant anti-growth ability against the assayed cancer cell lines, particularly against BGC-823, while low cytotoxicity to human normal gastric cell line GES-1. Further investigation revealed that UA-1a could induce apoptotic events of the treated BGC-823 cells, such as comet-like DNA bend, sub-G0/G1 phase accumulation and phosphatidylserine externalization. The activity of Caspase-3 was found to be up-regulated, while the expression of Bcl-2 and Survivin were down-regulated in UA-1a treated cells. UA-1a might trigger the death of BGC-823 cells by inducing apoptosis via the mitochondria pathway. UA-1a exerted stronger ability than Taxol to retard tumor growth in nude mice without leaving apparent toxicity to the hosts. The experimental data suggested that UA-1a would have a therapeutic potential in the treatment of gastric cancer.     

TAT Modification of Alpha-Helical Anticancer Peptides to Improve Specificity and Efficacy

HPRP-A1 is an amphipathic α-helical anticancer peptide (ACP) derived from the N-terminus of ribosomal protein L1 (RpL1) of Helicobacter pylori. In our previously study, HPRP-A1 has been reported that induced HeLa cell apoptosis in a caspase-dependent approach and involved both by the death receptor ‘extrinsic’ pathway and the mitochondria ‘intrinsic’ pathway. Here we report the construction of a new hybrid peptide, HPRP-A1-TAT, comprising the cell-permeating peptide TAT linked to the C-terminus of HPRP-A1. This peptide exhibits higher anticancer activity against HeLa cells with lower toxicity against human RBC than HPRP-A1. Two FITC-labeled peptides, FITC-HPRP-A1 and FITC-HPRP-A1-TAT, were used to investigate and compare the cellular uptake mechanism using fluorescence spectra and flow cytometry. Compared with HPRP-A1, HPRP-A1-TAT quickly crossed cell, entered the cytoplasm via endocytosis, and disrupted the cell membrane integrity. HPRP-A1-TAT exhibited stronger anticancer activity than HPRP-A1 at the same concentration by increasing early apoptosis of HeLa cells and inducing caspase activity. Notably, after 24 h, the cellular concentration of HPRP-A1-TAT was higher than that of HPRP-A1. This result suggests that TAT protects HPRP-A1 against degradation, likely due to its high number of positively charged amino acids or the further release of peptides into cancer cells from endocytotic vesicles. We believe that this TAT modification approach may provide an effective new strategy for improving the therapeutic index and anticancer activity of ACPs for clinical use.     

Raddeanin A induces human gastric cancer cells apoptosis and inhibits their invasion in vitro

Raddeanin A is one of the triterpenoid saponins in herbal medicine Anemone raddeana Regel which was reported to suppress the growth of liver and lung cancer cells. However, little was known about its effect on gastric cancer (GC) cells. This study aimed to investigate its inhibitory effect on three kinds of different differentiation stage GC cells (BGC-823, SGC-7901 and MKN-28) in vitro and the possible mechanisms. Proliferation assay and flow cytometry demonstrated Raddeanin A’s dose-dependent inhibitory effect and determined its induction of cells apoptosis, respectively. Transwell assay, wounding heal assay and cell matrix adhesion assay showed that Raddeanin A significantly inhibited the abilities of the invasion, migration and adhesion of the BGC-823 cells. Moreover, quantitative real time PCR and Western blot analysis found that Raddeanin A increased Bax expression while reduced Bcl-2, Bcl-xL and Survivin expressions and significantly activated caspase-3, caspase-8, caspase-9 and poly-ADP ribose polymerase (PARP). Besides, Raddeanin A could also up-regulate the expression of reversion inducing cysteine rich protein with Kazal motifs (RECK), E-cadherin (E-cad) and down-regulate the expression of matrix metalloproteinases-2 (MMP-2), MMP-9, MMP-14 and Rhoc. In conclusion, Raddeanin A inhibits proliferation of human GC cells, induces their apoptosis and inhibits the abilities of invasion, migration and adhesion, exhibiting potential to become antitumor drug.