Glehnia littoralis Root Extract Induces G0/G1 Phase Cell Cycle Arrest in the MCF-7 Human Breast Cancer Cell Line

Glehnia littoralis (GL) is widely used as an oriental medicine for cough, fever, stroke and other disease conditions. However, the anti-cancer properties of GL on MCF-7 human breast cancer cells have not been investigated. In order to elucidate anti-cancer properties and underlying cell death mechanisms, MCF-7cells (5 X 104/well) were treated with Glehnia littoralis root extract at 0-400 ug/ml. A hot water extract of GL root inhibited the proliferation of MCF-7 cells in a dose-dependent manner. Analysis of the cell cycle after treatment of MCF-7 cells with increasing concentrations of GL root extract for 24 hours showed significant cell cycle arrest in the G1 phase. RT-PCR and Western blot analysis both revealed that GL root extract significantly increased the expression of p21 and p27 with an accompanyingdecrease in both CDK4 and cyclin D1. Our reuslts indicated that GL root extract arrested the proliferation of MCF-7 cells in G1 phase through inhibition of CDK4 and cyclin D1 via increased induction of p21 and p27. In summary, the current study showed that GL could serve as a potential source of chemotherapeutic or chemopreventative agents against human breast cancer.     

HER2/neu受体酪氨酸激酶抑制剂SUCI02对乳腺癌细胞周期的影响及其分子机理

目的:探讨SUCI02对HER2受体过表达的乳腺癌细胞周期分布的影响及其分子机制.方法:采用免疫印迹法检测蛋白表达量和磷酸化蛋白量的变化;流式细胞术检测细胞周期的分布.RT-PCR检测mRNA的表达.结果:SUCI02处理MDA-MB-453细胞24h后,流式细胞仪分析可见在0、2.5、5、10、20μg/ml浓度下,MDA-MB-453细胞G0/G1期分别为:59.5%、65.8%、68.2%、70.0%、79.0%;S期分别为:38.1%、31.9%、29.4%、27.4%、18.3%;G2M期分别为:2.4%、2.3%、2.4%、2.6%、2.7%.不同浓度的SUCI02处理MDA-MB-453细胞24h后,细胞中p27上调,Rb的高磷酸化状态下降,Cvclin D1蛋白水平在10、20μg/ml SUCI02作用下显著下降.RT-PCR检测结果可见SUCI02对Cyclin D1的mRNA表达有明显的抑制作用.结论:SUCI02能诱导HER2/neu过表达的乳腺癌MDA-MB-453细胞停止于G1期,且与p27上调、Rb的高磷酸化状态下降、Cyclin D1 mRNA和蛋白水平下降有关.     

Vitexicarpin Induces Apoptosis in Human Prostate Carcinoma PC-3 Cells through G2/M Phase Arrest

Vitexicarpin (3’, 5-dihydroxy-3, 4’, 6, 7-tetramethoxyflavone), a polymethoxyflavone isolated from ViticisFructus (Vitex rotundifolia Linne fil.), has long been used as an anti-inflammatory herb in traditional Chinesemedicine. It has also been reported that vitexicarpin can inhibit the growth of various cancer cells. However,there is no report elucidating its effect on human prostate carcinoma cells. The aim of the present study was toexamine the apoptotic induction activity of vitexicarpin on PC-3 cells and molecular mechanisms involved. MTTstudies showed that vitexicarpin dose-dependently inhibited growth of PC-3 cells with an IC50~28.8 μM. Hoechst33258 staining further revealed that vitexicarpin induced apoptotic cell death. The effect of vitexicarpin on PC-3cells apoptosis was tested using prodium iodide (PI)/Annexin V-FITC double staining and flow cytometry. Theresults indicated that vitexicarpin induction of apoptotic cell death in PC-3 cells was accompanied by cell cyclearrest in the G2/M phase. Furthermore, our study demonstrated that vitexicarpin induction of PC-3 cell apoptosiswas associated with upregulation of the proapoptotic protein Bax, and downregulation of antiapoptotic proteinBcl-2, release of Cytochrome c from mitochondria and decrease in mitochondrial membrane potential. Ourfindings suggested that vitexicarpin may become a potential leading drug in the therapy of prostate carcinoma.     

Calotroposid A: a Glycosides Terpenoids from Calotropis gigantea Induces Apoptosis of Colon Cancer WiDr Cells through Cell Cycle Arrest G2/M and Caspase 8 Expression

Objective: This study aims to isolate the active anticancer compound from ethyl acetate fraction extracted fromthe roots of Calotropis gigantea and to determine the operating mechanism of the isolates towards WiDr colon cancercells. Methods: the isolation was conducted by using bioassay guided isolation approach method. The cytotoxicpotential was determined by using MTT method. The chemical structure was identified by using UPLCMS/MS andNMR-1H spectroscopy. The cell cycle arrest and apoptosis induction were determined by flow cytometry method.The expression of caspase-8 was determined by immunocytochemistry method. Results: The results showed thatthe active compounds are obtained calotroposid A compound which is glycosides terpenoids. Calotroposide Ais capable of inhibiting the growth of WiDr colon cancer cells at IC50 17.23μg/ml. Cell apoptosis induction took placeand was indicated by cell apoptosis increase, S and G2/M accumulation and by caspase-8 expression. Conclusion:Calotroposide A induces anticancer activity against WiDr colon cancer cells by means of apoptosis induction mechanismthrough extrinsic pathway with increased expression of caspase-8.     

Downregulation of Cdk1 and CyclinB1 Expression Contributes to Oridonin-induced Cell Cycle Arrest at G2/M Phase and Growth Inhibition in SGC-7901 Gastric Cancer Cells

Background: Oridonin isolated from Rabdosia rubescens, a plant used to treat cancer in Chinese folk medicine, is one of the most important antitumor active ingredients. Previous studies have shown that oridonin has antitumor activities in vivo and in vitro, but little is known about cell cycle effects of oridonin in gastric cancer. Materials and Methods: MTT assay was adopted to detect the proliferation inhibition of SGC-7901 cells, the cell cycle was assessed by flow cytometry and protein expression by Western blotting. Results: Oridonin couldinhibit SGC-7901 cell proliferation, the IC50 being 15.6 μM, and blocked SGC-7901 cell cycling in the G2/M phase. The agent also decreased the protein expression of cyclinB1 and CDK1. Conclusions: Oridonin may inhibit SGC-7901 growth and block the cells in the G2/M phase by decreasing Cdk1 and cyclinB1 proteins.     

芹菜素诱导乳腺癌T47D细胞系p53依赖性凋亡及G2/M期阻滞

  目的  探讨芹菜素（apigenin）对乳腺癌T47D细胞系凋亡及细胞周期的影响。  方法  常规培养T47D细胞, 用四甲基偶氮唑盐法（MTT法）检测芹菜素对乳腺癌T47D细胞系细胞增殖的影响。荧光染色法观察凋亡细胞的形态变化。流式细胞仪检测细胞凋亡率及周期分布。Western blot检测不同浓度（0、10、20、40、80 μM）芹菜素对凋亡及周期相关蛋白表达的影响。  结果  随着芹菜素浓度的增加, 芹菜素对T47D细胞的增殖抑制作用明显增强（P < 0.05）; 凋亡荧光染色及流式细胞仪显示, 芹菜素能够诱导乳腺癌T47D细胞凋亡, 随着其浓度的增高, 各组凋亡率分别为（2.41±0.072）%、（10.87±0.028）%、（18.02±0.056）%、（37.05± 0.092）%和（78.38±0.082）%, 与对照组相比, 差异有统计学意义（P < 0.05）; 流式周期分析显示, 芹菜素能够使T47D细胞系G₂/M期阻滞, 随着芹菜素浓度的增高, 不同浓度组细胞G₂/M期所占的比例逐渐增加, 差异有统计学意义（P < 0.05）; Western blot显示p53、p21、Bax和p-Cdc2的含量及Caspase-3, PARP剪切明显增加, 而Bcl-2、CyclinB1及Cdc2的含量却显著减少。  结论  芹菜素能够诱导乳腺癌T47D细胞系p53依赖性凋亡及G₂/M期阻滞, 从而明显抑制其增殖。      

Inhibition of JAK1, 2/STAT3 Signaling Induces Apoptosis, Cell Cycle Arrest, and Reduces Tumor Cell Invasion in Colorectal Cancer Cells

Abnormalities in the STAT3 pathway are involved in the oncogenesis of several cancers. However, the mechanism by which dysregulated STAT3 signaling contributes to the progression of human colorectal cancer (CRC) has not been elucidated, nor has the role of JAK, the physiological activator of STAT3, been evaluated. To investigate the role of both JAK and STAT3 in CRC progression, we inhibited JAK with AG490 and depleted STAT3 with a SiRNA. Our results demonstrate that STAT3 and both JAK1 and 2 are involved in CRC cell growth, survival, invasion, and migration through regulation of gene expression, such as Bcl-2, p1^6ink4a, p21^waf1/cip1, p27^kip1, E-cadherin, VEGF, and MMPs. Importantly, the FAK is not required for STAT3-mediated regulation, but does function downstream of JAK. In addition, our data show that proteasome-mediated proteolysis promotes dephosphorylation of the JAK2, and consequently, negatively regulates STAT3 signaling in CRC. Moreover, immunohistochemical staining reveals that nuclear staining of phospho-STAT3 mostly presents in adenomas and adenocarcinomas, and a positive correlation is found between phospho-JAK2 immunoreactivity and the differentiation of colorectal adenocarcinomas. Therefore, our findings illustrate the biologic significance of JAK1, 2/STAT3 signaling in CRC progression and provide novel evidence that the JAK/STAT3 pathway may be a new potential target for therapy of CRC.     

Kaempferol Suppresses Proliferation and Induces Cell Cycle Arrest,Apoptosis, and DNA Damage in Breast Cancer Cells

Kaempferol is a flavonoid that has been extensively investigated owing to its antitumor effects. Nevertheless, little is known about its underlying mechanisms of action. We aimed to explore the role of kaempferol in breast cancer (BC), and thus we investigated how kaempferol suppresses the growth of BC cells. The cells were treated with kaempferol, and the effects on multiple cancer-associated pathways were evaluated. The MTS assay was used to study the cell growth inhibition induced by kaempferol. The cell cycle was analyzed by flow cytometry. Western blotting was used to analyze cellular apoptosis and DNA damage. We found that the proliferation of the triple-negative BC (TNBC) MDA-MB-231 cells was suppressed effectively by kaempferol. Interestingly, the suppressive effect of kaempferol on cell proliferation was stronger in MDA-MB-231 cells than in the estrogen receptor-positive BT474 cell line. Furthermore, after the treatment with kaempferol for 48 h, the population of cells in the G1 phase was significantly reduced, from 85.48% to 51.35%, and the population of cells in the G₂ phase increased markedly from 9.27% to 37.5%, which indicated that kaempferol contributed to the induction of G₂/M arrest. Kaempferol also induced apoptosis and DNA damage in MDA-MB-231 cells. Kaempferol increased the expression levels of H2AX, cleaved caspase 9, cleaved caspase 3, and p-ATM compared to those of the control group. Collectively, these results showed that kaempferol may be a potential drug for the effective treatment of TNBC.     

选择性COX-2抑制剂Celecoxib诱导胶质瘤细胞凋亡作用机制初探

背景与目的：选择性COX-2抑制剂具有诱导多种肿瘤细胞凋亡的作用，但在胶质瘤方面研究还不多见，本研究门的是探讨选择忡COX-2抑制剂塞来昔布（Celecoxib）诱导胶质瘤C6细胞凋亡，及其在诱导胶质瘤细胞凋亡的作用机制方法：应州PGE2检测、吖啶橙染色、流式细胞仪（FCM）检测不同浓度的Celecoxib对胶质瘤C6细胞作用，通过放免法检测不同浓度Celecoxib作用于胶质瘤C6细胞后PGE2的含量，通过吖啶橙染色从形态上观察治疗组细胞的形态学变化，流式细胞仪检测各组细胞发生凋亡的情况。结果：随Celecoxib浓度增加而PGE2合成减少（P〉0．05）．吖啶橙染色荧光染色对照组细胞核DNA为均匀黄色或黄绿色的荧光，治疗组（Celecoxib 50μmol／L）凋亡细胞的细胞核或细胞质内可处致密浓染的黄绿色荧光或黄绿色碎片．Celecoxib浓度为12．5μmol／L和50μmol／L时．FCM法检测凋亡分别为5．83％和15．32％．Celecoxib对C6胶质瘤细胞增殖抑制作用具有浓度依赖性．细胞凋亡随浓度增加而增多。结论：Celecoxib具有诱导胶质瘤C6细胞凋亡的作用并呈剂量依赖性，随PGE2合成下降细胞凋亡增多，PGE2途径是Celecoxib诱导胶质瘤细胞凋亡机制之一．对胶质瘤的治疗有重要意义。     

选择性COX-2抑制剂Celecoxib对胃癌细胞增殖影响的探讨

目的:探讨选择性COX-2抑制剂Celecoxib对胃癌SGC-7901细胞增殖和凋亡的影响.方法:应用MTT法和FCM检测Celecoxib对胃癌SGC-7901细胞增殖、细胞凋亡、细胞周期和COX-2蛋白和bcl-2蛋白表达的影响.结果:Celecoxib呈时间、剂量依赖性抑制胃癌SGC-7901细胞生长,72h细胞最高存活率为48.7%,最低为20.5%;COX-2蛋白含量由26.73±0.06降至5.79±1.44,bcl-2蛋白含量由2.76±0.14降至0.78±0.05,COX-2蛋白和bcl-2蛋白表达的降低呈浓度依赖性;随着药物浓度的增高,细胞凋亡率由3.0%增加到33.0%;G0/G1期细胞比例增加到(87.29±1.34)%,S期和G2/M期细胞比例分别降低到(8.91±0.78)%、(3.80±0.55)%.结论:Celecoxib能够诱导胃癌SGC-7901细胞的凋亡,影响细胞周期的分布,从而有效地抑制胃癌SGC-7901细胞的增殖;Celecoxib诱导胃癌SGC-7901细胞的凋亡可能主要通过抑制COX-2的生物活性来实现,并与bcl-2蛋白表达的下调有关.     

Curcumin Analogue A501 induces G2/M Arrest and Apoptosis in Non-small Cell Lung Cancer Cells

Curcumin and its analogues have been reported to exert anti-cancer activity against a variety of tumors. Here, we reported A501, a new curcumin analogue. The effect of A501 on cell viability was detected by MTT assay, the result showed that A501 had a better inhibiting effect on the four non-small cell lung cancer (NSCLC) cells than that of curcumin. Moreover, Colony forming experiment showed A501 significant restrained cell proliferation. Flow cytometry displayed A501 can cause G2/M arrest and induce apoptosis. Western blotting showed thatA501 decreased the expression of cyclinB1, cdc-2, bcl-2, while increased the expression of p53, cleaved caspase-3 and bax. In conclusion, curcumin analogues A501 played antitumor activity by inhibiting cell proliferation andinducing apoptosis of NSCLC cells. And it was likely to be a promising starting point for the development of curcumin-based anticancer drugs.     

Induction of Apoptotic Death and Cell Cycle Arrest in HeLa Cells by Extracellular Factors of Breast Cancer Cells

Background: There are evidences on the role of extracellular factors in cellular communication between cancercells and non-cancerous cells to support tumor progression and a phenomenon of cancer cachexia. However, evidencesare scarce to show the effects of extracellular factors from one carcinoma microenvironment upon growth and survivalof another carcinoma. Methodology: To address the above issue, we have selected excised breast carcinoma tissuesamples and in vitro grown MCF-7 sources of extracellular factors and tested their effects to evaluate growth andproliferation inhibitory potential against a cervical carcinoma cell line HeLa. Results: Data from the in vitro experimentslike Trypan blue dye exclusion, MTT assay, cell cycle assay and annexin V/PI staining lead us to suggest that theextracellular factors collected from the culture medium of in vitro grown MCF-7 and excised breast carcinoma tissueplay an apoptosis inducing and cell cycle arrest role in HeLa. In these in vitro experiments, we detected the presence ofup to 40-50% apoptotic cell death in HeLa cells and increase in G2-M cell cycle phase from 11%-25% due to treatmentwith extracellular factors from human breast carcinoma cells. Discussion and Conclusion: These observations arenovel and suggest that extracellular factors from breast carcinoma play an apoptosis inducing and growth inhibitoryrole upon on HeLa cells. This study can also support the concept of cancer cachexia and a possible hypothesis for rarechance of synchronous two or more primary tumor in a single patient.     

塞来昔布诱导Ls174结肠腺癌细胞周期阻滞和凋亡

目的：观察选择性COX-2抑制剂塞来昔布（Celecoxib）诱导结肠腺癌细胞株Ls174凋亡的作用及机制。方法：采用MTT法检测塞来昔布对Ls174细胞的增殖抑制作用，应用流式细胞仪检测塞来昔布对Ls174细胞凋亡和增殖周期的影响．并检测塞来昔布对Ls174细胞Caspase-3活性的影响。结果：塞来昔布抑制Ls174细胞增殖和诱导Ls174细胞的凋亡作用均呈剂量和时间依赖性，塞来昔布处理后的Ls174细胞G0／G1期百分比与对照组相比明显增高。塞来昔布能诱导Ls174细胞Caspase-3活性，并呈浓度和时间依赖性。结论：塞来昔布在体外能抑制Ls174细胞的增殖。诱导细胞凋亡，其作用与促进Caspase-3活性和阻滞细胞周期于G0／G1期有关。     

二烯丙基二硫化物诱导胃癌BGC823 细胞周期G2/M期阻滞的机制*

目的:以细胞周期作为抗癌药物新靶点的研究,可能是很有前途的。笔者的前期工作发现,二烯丙基二硫化物（diallyl disulfide,DADS）可抑制人胃癌BGC 823 细胞增殖,其增殖抑制与细胞周期G2/M期阻滞有关;DADS可能是通过抑制细胞分裂周期蛋白25C（Cell division cycle protein 25C,Cdc25C）、cyclinB 1 表达使部分BGC 823 细胞停滞在G2/M期,但G2/M期阻滞的机制还未完全阐明。本研究进一步探讨DADS诱导人胃癌BGC 823 细胞周期G2/M期阻滞的可能机制。方法:RT-PCR 检测Chk1 和Chk2 在mRNA 水平的改变;Western blot检测DADS处理BGC 823 细胞前后细胞周期相关蛋白ATM-RAD3 相关基因（ATM-RAD3-related gene,ATR ）、细胞周期检查点蛋白激酶1（checkpoint kinase1,Chk1）、细胞周期检查点蛋白激酶2（checkpoint kinase2,Chk2）表达和ATR 、Chk1、Chk2 的磷酸化程度;免疫共沉淀检测Chk1、Chk2 与Cdc25C 结合情况。结果:RT-PCR 检测显示,Chk1 和Chk2 的mRNA 水平在处理组与未处理组之间无显著性差异（P>0.05）。 Western blot检测显示,总Chk1 和Chk2 蛋白表达在细胞处理前后均无明显改变,但15mg/LDADS刺激BGC 823 细胞2h 后,处理组细胞Chk1 磷酸化程度明显增加,并呈时间依赖性（P<0.05）,而Chk2 磷酸化程度在处理组与未处理组之间无显著性差异（P>0.05）。 15mg/L DADS 作用15～120min,ATR 磷酸化程度明显增加,呈时间依赖性（P<0.05）,而ATR 表达无改变。免疫共沉淀分析表明,DADS 能促进BGC 823 细胞Chk1 与Cdc25C 结合,而对Chk2 与Cdc25C 结合无影响。结论:DAD诱导人胃癌BGC 823 细胞G2/M期阻滞与Chk1 的活化有关,DADS可能是通过激活ATR 、Chk1,调节Cdc25C 的表达引起人胃癌BGC 823 细胞G2/M期阻滞。      

LY294002 Induces G0/G1 Cell Cycle Arrest and Apoptosis of Cancer Stem-like Cells from Human Osteosarcoma Via Downregulation of PI3K Activity

Osteosarcoma, the most common primary mesenchymal malignant tumor, usually has bad prognosis inman, with cancer stem-like cells (CSCs) considered to play a critical role in tumorigenesis and drug-resistance.It is known that phosphatidylinositol 3-kinase (PI3K) is involved in regulation of tumor cell fates, such asproliferation, cell cycling, survival and apoptosis. Whether and how PI3K and inhibitors might cooperate inhuman osteosarcoma CSCs is still unknown. We therefore evaluated the effects of LY294002, a PI3K inhibitor,on the cell cycle and apoptosis of osteosarcoma CSCs in vitro. LY294002 prevented phosphorylation of proteinkinase B (PKB/Akt) by inhibition of PI3K phosphorylation activity, thereby inducing G0/G1 cell cycle arrest andapoptosis in osteosarcoma CSCs. Further studies also demonstrated that apoptosis induction by LY294002 isaccompanied by activation of caspase-9, caspase-3 and PARP, which are involved in the mitochondrial apoptosispathway. Therefore, our results indicate PI3K inhibitors may represent a potential strategy for managing humanosteosarcoma via affecting CSCs.     

乳腺癌中COX-2表达及其抑制剂塞来昔布对乳腺癌细胞系增生和凋亡的影响

目的为进一步观察COX-2对乳腺癌的作用,我们检测了乳腺癌组织、乳腺癌细胞株MCF-7和B37中COX-2的表达,并观察选择性COX-2抑制剂塞来昔布对乳腺癌细胞株生长和凋亡的影响。方法应用免疫组织化学染色的方法检测132例乳腺癌组织标本中COX-2蛋白的表达;应用免疫细胞化学染色、原位杂交、逆转录多聚酶联反应（RT-PCR）的方法,分别检测COX-2蛋白和mRNA在乳腺癌细胞株MCF-7、B37中的表达;采用MTT法、AO/EB双荧光染色法和流式细胞术,研究塞来昔布对乳腺癌细胞增殖和凋亡的影响。结果52.3%(69/132)的乳腺癌组织标本表达COX-2蛋白;在乳腺癌细胞株MCF-7和B37中均有COX-2的表达,25μmol/L塞来昔布作用72h后,COX-2表达明显减少;25、50、100μmol/L的塞来昔布与MCF-7细胞作用72h,生长抑制率分别为36.3%、57.7%、74.5%。100μmol/L塞来昔布作用72h后,MCF-7细胞凋亡率为38.5％。结论乳腺癌组织和乳腺癌细胞株MCF-7、B37中存在COX-2的表达;塞来昔布可抑制乳腺癌细胞增殖,并促进细胞凋亡,塞来昔布可能作为新的药物治疗乳腺癌。     

选择性COX-2抑制剂塞来昔布对乳腺癌的放疗增敏作用及其机制研究

[目的]探讨选择性环氧化酶-2（COX-2）抑制剂塞来昔布对人乳腺癌细胞的放疗增敏作用及其可能的机制。[方法]取对数生长期MDA-MB-231细胞株,实验分为对照组、药物组、照射组及实验组（照射线＋塞来昔布）。流式细胞术（FCM）检测细胞周期变化和各组凋亡率;克隆形成实验检测放射增敏作用;Western blot法检测COX-2、VEGF、Bcl-2蛋白表达。[结果]不同浓度塞来昔布对MDA-MB-231细胞有明显抑制作用,且呈剂量依赖性（F=5.56,P=0.030）。FCM检测结果显示,随塞来昔布浓度增加,细胞周期明显变化（G0/G1期比例增高,S期比例降低）。实验组凋亡率较照射组明显高（31.20%±1.27%vs 17.99%±1.01%,t=2.43,P=0.025）。克隆形成实验显示,实验组与照射组相比较,反映放射敏感性指标的Dq、Do和SF2显著降低。塞来昔布能抑制COX-2、VEGF和Bcl-2蛋白表达（P〈0.05）。[结论]选择性COX-2抑制剂塞来昔布对人乳腺癌MDA-MB-231细胞有明显的放射增敏作用,其可能的机制是抑制COX-2表达、诱导细胞凋亡、调节细胞周期分布和抑制细胞血管生成因子生成。     

环氧化酶-2抑制剂塞来昔布对胃癌端粒酶活性影响的体内外实验研究

目的 探讨选择性环氧合酶-2 （COX-2）抑制剂塞来昔布对SGC-7901人胃癌细胞及裸鼠移植瘤的生长、端粒酶活性及相关因素的影响,研究其抗肿瘤的作用机制.方法 终浓度为100,200,及300 μmol/L的塞来昔布作用于SGC-7901人胃癌细胞,同时建立裸鼠胃癌模型,20只裸鼠随机分为两组,对照组隔日腹腔注射生理盐水,塞来昔布组隔日腹腔注射塞来昔布30 mg/kg,采用MTT比色法测定胃癌细胞的生长抑制率,采用半定量-TRAP银染法检测SGC-7901人胃癌细胞及裸鼠移植瘤组织中的端粒酶活性.结果 不同浓度的塞来昔布对SGC-7901人胃癌细胞的生长均有抑制作用,抑制率与对照组相比,差异有显著性（P〈0.05）;塞来昔布组裸鼠肿瘤生长明显受抑制,抑瘤率为61.3%,与对照组相比,差异有显著性（P〈0.05）;同时塞来昔布也显著抑制SGC-7901人胃癌细胞及裸鼠移植瘤组织中的端粒酶活性,其抑制作用呈时间-剂量依赖性.结论 塞来昔布通过降低端粒酶活性,诱导细胞凋亡,抑制细胞增殖,从而参与抑制胃癌生长,这可能是COX-2抑制剂体内抗胃癌的机制之一.