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Role of cyclooxygenase-2 in gastric cancer development and progression 被引量:33
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作者 Jian Cheng Xiao-Ming Fan 《World Journal of Gastroenterology》 SCIE CAS 2013年第42期7361-7368,共8页
Although the incidence of gastric cancer has been declining in recent decades,it remains a major public health issue as the second leading cause of cancer death worldwide.In China,gastric cancer is still the main caus... Although the incidence of gastric cancer has been declining in recent decades,it remains a major public health issue as the second leading cause of cancer death worldwide.In China,gastric cancer is still the main cause of death in patients with malignant tumors.Most patients are diagnosed at an advanced stage and mortality is high.Cyclooxygenase-2(COX-2)is a ratelimiting enzyme in prostanoid synthesis and plays an important role in the development and progression of gastric cancer.The expression of COX-2 in gastric cancer is upregulated and its molecular mechanisms have been investigated.Helicobacter pylori infection,tumor suppressor gene mutation and the activation of nuclear factor-kappa B may be responsible for the elevated expression of COX-2 in gastric cancer.The mechanisms of COX-2 in the development and progression of gastric cancer are probably through promoting the proliferation of gastric cancer cells,while inhibiting apoptosis,assisting angiogenesis and lymphatic metastasis,and participating in cancer invasion and immunosuppression.This review is intended to discuss,comment and summarize recent research progress on the role of COX-2 in gastric cancer development and progression,and elucidate the molecular mechanisms which might be involved in the carcinogenesis. 展开更多
关键词 cyclooxygenase-2 gastric cancer Prostagladin CARCINOGENESIS MOLECULAR mechanism
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Interaction between cyclooxygenase-2,Snail,and E-cadherin in gastric cancer cells 被引量:8
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作者 Xiao-Jun Liu Zhao-Feng Chen +7 位作者 Hai-Long Li Ze-Nan Hu Min Liu Ai-Ping Tian Da Zhao Jing Wu Yong-Ning Zhou Liang Qiao 《World Journal of Gastroenterology》 SCIE CAS 2013年第37期6265-6271,共7页
AIM:To investigate the mechanisms of how cyclooxygenase-2(COX-2)regulates E-cadherin in gastric cancer cells.METHODS:COX-2 expression in human gastric cancer cell lines SGC-7901,BGC-823,MGC-803 and AGS were measured a... AIM:To investigate the mechanisms of how cyclooxygenase-2(COX-2)regulates E-cadherin in gastric cancer cells.METHODS:COX-2 expression in human gastric cancer cell lines SGC-7901,BGC-823,MGC-803 and AGS were measured at the mRNA and protein level.COX-2 rich cell line SGC-7901 was chosen for subsequent experiments.siRNA mediated gene knockdown was used to investigate the impact of COX-2 on nuclear factor-κB (NF-κB),Snail,and E-cadherin in gastric cancer cells.Gene expression was determined by Western blot and real-time polymerase chain reaction.To analyze whether NF-κB inhibition could interrupt the modulatory effect of COX-2 or prostaglandin E2(PGE2)on E-cadherin,gastric cancer cells were treated with celecoxib or PGE2,in the presence of NF-κB specific siRNA.RESULTS:Highest expression level of COX-2 was found in SGC-7901 cells,both at mRNA and protein levels.siRNA mediated down-regulation of COX-2 led to a reduced expression of NF-κB and Snail,but an increased expression of E-cadherin in SGC-7901 cells.siRNA mediated down-regulation of NF-κB also led to a reduced expression of E-cadherin and Snail in SGC-7901 cells.However,COX-2 expression did not alter after cells were treated with NF-κB specific siRNA in SGC-7901 cells.Treatment of SGC-7901 cells with celecoxib led to a reduced expression of Snail but an increased expression of E-cadherin.In contrast,treatment of SGC-7901 cells with PGE2 led to an increased Snail and a decreased E-cadherin.However,siRNAmediated knockdown of NF-κB partially abolished the effect of celecoxib and PGE2 on the regulation of E-cadherin and Snail in SGC-7901 cells.CONCLUSION:COX-2 likely functions upstream of NF-κB and regulates the expression of E-cadherin via NF-κB/Snail signaling pathway in gastric cancer cells. 展开更多
关键词 cyclooxygenase-2 E-CADHERIN CELECOXIB PROSTAGLANDIN E2 gastric cancer
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Expression of cyclooxygenase-2 in gastric cancer and its relation to liver metastasis and long-term prognosis 被引量:12
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作者 Ji-Ren Yu Yi-Jun Wu +4 位作者 Qi Qin Ke-Zheng Lu Sheng Yan Xiao-Sun Liu Shu-Sen Zheng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第31期4908-4911,共4页
AIM: To investigate the expression of cyclooxygenase-2(COX-2) in gastric cancer and its relation with the liver metastasis and prognosis.METHODS: Expression of COX-2 mRNA and protein was examined in gastric cancer and... AIM: To investigate the expression of cyclooxygenase-2(COX-2) in gastric cancer and its relation with the liver metastasis and prognosis.METHODS: Expression of COX-2 mRNA and protein was examined in gastric cancer and its paired substantial normal tissue by semi-quantitative reverse transcriptionpolymerase chain reaction and immunohistochemistry.The relation between COX-2 expression and prognosis was investigated in 195 cases.RESULTS: The expression of COX-2 mRNA in gastric cancer tissue was significantly higher than that in normal tissue in 47 cases (w= 792, P<0.01). The COX-2 mRNA in pT3-4 tissue expressed higher than that in pT1-2tissue (w = 204, P<0.05). The positive expression rate of COX-2 protein was 57.9% (113/195). The COX-2expression was significantly related to histological type,lymphnode metastasis, venous invasion and liver metastasis (P<0.05). No relation was found between COX-2 expression and invasion depth, peritoneal metastasis and International Union against Cancer TNMstage. The multiple regression analysis showed that the COX-2 expression and venous invasion were obviously associated with liver metastasis (P<0.05). However,there was no significant correlation between COX-2immunoreactivity and prognosis.CONCLUSION: COX-2 may play an important role in the development of gastric cancer, and the over-expression of COX-2 protein may be a high risk factor for liver metastasis. 展开更多
关键词 gastric cancer cyclooxygenase-2 Neoplasm metastasis Long-term prognosis
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Genetic variant of cyclooxygenase-2 in gastric cancer:More inflammation and susceptibility 被引量:6
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作者 Xuan-Ke Ji Sailaja Vatsalya Madhurapantula +4 位作者 Gui He Kun-Yan Wang Chun-Hua Song Jian-Ying Zhang Kai-Juan Wang 《World Journal of Gastroenterology》 SCIE CAS 2021年第28期4653-4666,共14页
Gastric cancer accounts for the majority cancer-related deaths worldwide.Although various methods have considerably improved the screening,diagnosis,and treatment of gastric cancer,its incidence is still high in Asia,... Gastric cancer accounts for the majority cancer-related deaths worldwide.Although various methods have considerably improved the screening,diagnosis,and treatment of gastric cancer,its incidence is still high in Asia,and the 5-year survival rate of advanced gastric cancer patients is only 10%-20%.Therefore,more effective drugs and better screening strategies are needed for reducing the incidence and mortality of gastric cancer.Cyclooxygenase-2(COX-2)is considered to be the key inducible enzyme in prostaglandins(PGs)synthesis,which is involved in multiple pathways in the inflammatory response.For example,inflammatory cytokines stimulate innate immune responses via Toll-like receptors and nuclear factor-kappa B to induce COX-2/PGE2 pathway.In these processes,the production of an inflammatory microenvironment promotes the occurrence of gastric cancer.Epidemiological studies have also indicated that non-steroidal antiinflammatory drugs can reduce the risk of malignant tumors of the digestive system by blocking the effect of COX-2.However,clinical use of COX-2 inhibitors to prevent or treat gastric cancer may be limited because of potential side effects,especially in the cardiovascular system.Given these side effects and low treatment efficacy,new therapeutic approaches and early screening strategies are urgently needed.Some studies have shown that genetic variation in COX-2 also play an important role in carcinogenesis.However,the genetic variation analysis in these studies is incomplete and isolated,pointing out only a few single nucleotide polymorphisms(SNPs)and the risk of gastric cancer,and no comprehensive study covering the whole gene region has been carried out.In addition,copy number variation(CNV)is not mentioned.In this review,we summarize the SNPs in the whole COX-2 gene sequence,including exons,introns,and both the 5’and 3’untranslated regions.Results suggest that COX-2 does not increase its expression through the CNV and the SNPs in COX-2 may serve as the potential marker to establish risk stratification in the general population.This review synthesizes emerging insights of COX-2 as a biomarker in multiple studies,summarizes the association between whole COX-2 sequence variation and susceptibility to gastric cancer,and discusses the future prospect of therapeutic intervention,which will be helpful for early screening and further research to find new approaches to gastric cancer treatment. 展开更多
关键词 cyclooxygenase-2 INFLAMMATION Genetic variant gastric cancer Prostaglandin E2
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Mechanism and clinical significance of cyclooxygenase-2 expression in gastric cancer 被引量:5
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作者 Bao-CanWang Chang-QingGuo +3 位作者 ChaoSun Qiao-LingSun Guo-YongLiu Ding-GuoLi 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第21期3240-3244,共5页
AIM: To determine the correlation between methylation status of 5' CpG island of cyclooxygenase-2 (COX-2) gene and protein expression in gastric cancer tissues for distinguishing the molecular characters of gastri... AIM: To determine the correlation between methylation status of 5' CpG island of cyclooxygenase-2 (COX-2) gene and protein expression in gastric cancer tissues for distinguishing the molecular characters of gastric cancers. METHODS: Methylation status of 5' CpG island of COX-2 gene was studied by PCR amplification after HpaⅡ and Hha I restrictive enzyme digestion;COX-2 expression was evaluated by immunohistochemical method. RESULTS: Hpa Ⅱ and HhaI site were all methylated in 12 normal gastric mucosa tissues, whereas they were demethylated in 77.27% (34/44) and 84.09% (37/44) gastric cancer tissues,respectively.Expression of COX-2 was detected in 68.18% (30/44) gastric cancer tissues, but no expression was found in normal gastric mucosa tissues. In gastric cancer tissues, COX-2 expression was correlated significantly with HpaⅡ site demethylation (29/30 vs 5/14, P<0.001 and HhaI site demethylation (28/30 vs 9/14,P<0.05). CONCLUSION: The demethylation of 5' CpG island of gene is necessary for COX-2 expression in human gastric cancer. The expression status of COX-2 may provide theoretical basis for COX-2 targeting gastric cancer treatments. 展开更多
关键词 gastric cancer METHYLATION cyclooxygenase-2
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Acetyl-11-keto-β-boswellic acid inhibits proliferation and induces apoptosis of gastric cancer cells through the phosphatase and tensin homolog/Akt/cyclooxygenase-2 signaling pathway 被引量:5
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作者 Meng-Xue Sun Xiao-Pu He +4 位作者 Pei-Yun Huang Qi Qi Wei-Hao Sun Gao-Shuang Liu Jie Hua 《World Journal of Gastroenterology》 SCIE CAS 2020年第38期5822-5835,共14页
BACKGROUND Gastric cancer is one of the most common malignant tumors of the digestive system worldwide,posing a serious danger to human health.Cyclooxygenase(COX)-2 plays an important role in the carcinogenesis and pr... BACKGROUND Gastric cancer is one of the most common malignant tumors of the digestive system worldwide,posing a serious danger to human health.Cyclooxygenase(COX)-2 plays an important role in the carcinogenesis and progression of gastric cancer.Acetyl-11-keto-β-boswellic acid(AKBA)is a promising drug for cancer therapy,but its effects and mechanism of action on human gastric cancer remain unclear.AIM To evaluate whether the phosphatase and tensin homolog(PTEN)/Akt/COX-2 signaling pathway is involved in the anti-tumor effect of AKBA in gastric cancer.METHODS Human poorly differentiated BGC823 and moderately differentiated SGC7901 gastric cancer cells were routinely cultured in Roswell Park Memorial Institute 1640 medium supplemented with 10%fetal bovine serum and 1%penicillin/streptomycin.Gastric cancer cell proliferation was determined by methyl thiazolyl tetrazolium colorimetric assay.Apoptosis was measured by flow cytometry.Cell migration was assessed using the wound-healing assay.Expression of Bcl-2,Bax,proliferating cell nuclear antigen,PTEN,p-Akt,and COX-2 were detected by Western blot analysis.A xenograft nude mouse model of human gastric cancer was established to evaluate the anti-cancer effect of AKBA RESULTS AKBA significantly inhibited the proliferation of gastric cancer cells in a dose-and time-dependent manner,inhibited migration in a time-dependent manner,and induced apoptosis in a dose-dependent manner in vitro;it also inhibited tumor growth in vivo.AKBA up-regulated the expression of PTEN and Bax,and downregulated the expression of proliferating cell nuclear antigen,Bcl-2,p-Akt,and COX-2 in a dose-dependent manner.The PTEN inhibitor bpv(Hopic)reversed the high expression of PTEN and low expression of p-Akt and COX-2 that were induced by AKBA.The Akt inhibitor MK2206 combined with AKBA downregulated the expression of p-Akt and COX-2,and the combined effect was better than that of AKBA alone.CONCLUSION AKBA inhibits the proliferation and migration and promotes the apoptosis of gastric cancer cells through the PTEN/Akt/COX-2 signaling pathway. 展开更多
关键词 Acetyl-11-keto-β-boswellic acid gastric cancer Cell proliferation APOPTOSIS cyclooxygenase-2 Tumor xenograft
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NS-398对人胃癌细胞株增殖及COX-2表达的影响 被引量:1
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作者 刘升云 李建生 张金平 《山东医药》 CAS 北大核心 2004年第13期17-18,共2页
目的 体外观察选择性环氧化酶 2 (COX- 2 )抑制剂 NS- 398对人胃癌细胞株 SGC790 1细胞增殖及COX- 2表达的影响。方法 采用噻唑蓝 (MTT)法观察 NS- 398对 SGC790 1细胞增殖的影响 ,流式细胞仪(FCM)研究 NS- 398对 SGC790 1细胞凋亡的... 目的 体外观察选择性环氧化酶 2 (COX- 2 )抑制剂 NS- 398对人胃癌细胞株 SGC790 1细胞增殖及COX- 2表达的影响。方法 采用噻唑蓝 (MTT)法观察 NS- 398对 SGC790 1细胞增殖的影响 ,流式细胞仪(FCM)研究 NS- 398对 SGC790 1细胞凋亡的作用 ,免疫细胞化学观察 COX- 2蛋白的表达。结果 体外 NS- 398能减少 SGC790 1细胞株 COX- 2的表达 ,对 SGC790 1有细胞毒作用 ,可增加细胞凋亡率。结论 体外 NS- 398对SGC790 1细胞增殖有抑制作用。可能与抑制 COX- 展开更多
关键词 ns-398 胃癌 增殖 COX-2 表达
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NS-398对人胃癌细胞系SGC-7901增殖、凋亡和COX-2表达的影响 被引量:2
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作者 余涛 李良庆 +2 位作者 王家兴 于锡阳 栗大伟 《肿瘤基础与临床》 2012年第1期1-5,共5页
目的探讨环氧合酶-2(COX-2)抑制剂NS-398对人胃癌细胞系SGC-7901增殖、凋亡及COX-2表达的影响,并进一步探讨其作用的可能机制。方法采用四甲基偶氮唑蓝(MTT)法检测NS-398对SGC-7901细胞的杀伤抑制作用;免疫细胞化学法检测SGC-7901细胞内... 目的探讨环氧合酶-2(COX-2)抑制剂NS-398对人胃癌细胞系SGC-7901增殖、凋亡及COX-2表达的影响,并进一步探讨其作用的可能机制。方法采用四甲基偶氮唑蓝(MTT)法检测NS-398对SGC-7901细胞的杀伤抑制作用;免疫细胞化学法检测SGC-7901细胞内COX-2的蛋白表达情况;ELISA法检测NS-398作用于SGC-7901细胞后PGE2释放水平;流式细胞仪检测SGC-7901细胞的凋亡情况。结果 NS-398对胃癌SGC-7901细胞具有较强的抑制作用,且这种抑制作用随浓度和时间的增加而增强,呈剂量-时间双效应关系(P<0.05);不同浓度NS-398作用下的SGC-7901细胞中,COX-2的表达明显减弱,且呈剂量梯度下降(P<0.05);NS-398可抑制PGE2释放,并且这种抑制作用呈剂量效应关系,与对照组相比差异有统计学意义(P<0.05);NS-398作用于SGC-7901细胞48 h后,细胞凋亡率升高,且呈剂量效应(P<0.05)。结论 NS-398通过COX-2依赖途径抑制SGC-7901细胞增殖并促进其凋亡。 展开更多
关键词 ns-398 胃癌细胞SGC-7901 增殖 凋亡 环氧合酶-2 前列腺素E2
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Specific COX-2 inhibitor NS398 induces apoptosis in human liver cancer cell line HepG2 through BCL-2 被引量:31
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作者 Dong-ShengHuang Ke-ZhenShen Jian-FengWei Thng-BoLiang Shu-SenZheng Hai-YangXie 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第2期204-207,共4页
AIM: To evaluate the effects of NS-398, a cyclooxygenase-2 (COX-2) inhibitor, on the proliferation and apoptosis of HepG2 cells. METHODS: The effects of NS-398 on the proliferation of HepG2 cells were evaluated by MTT... AIM: To evaluate the effects of NS-398, a cyclooxygenase-2 (COX-2) inhibitor, on the proliferation and apoptosis of HepG2 cells. METHODS: The effects of NS-398 on the proliferation of HepG2 cells were evaluated by MTT. DNA fragmentation gel analysis was used to analyze the apoptotic cells. DNA ploidy and apoptotic cell percentage were calculated by flow cytornetry. The expression of COX-2 and Bcl-2 mRNA was identified by competitive RT-PCR. Furthermore, expression level of Bcl-2 was detected using Western blot in HepG2 after treated with NS-398. RESULTS: NS-398 inhibited cell proliferation and induced apoptosis of HepG2 cells in a concentration-dependent manner. DNA ploidy analysis showed that S phase cells were significantly decreased with increase of NS-398 concentration. The quiescent GO/G1 phase was accumulated with decrease of Bcl-2 mRNA. Whereas NS-398 had no effect on the expression of COX-2 mRNA, and no correlations were found between COX-2 mRNA and HepG2 cell proliferation and apoptosis induced by NS-398 (r=0.056 and r=0.119, respectively). Bcl-2 protein level was inhibited after treated with NS-398. CONCLUSION: NS-398 significantly inhibits the proliferation and induces apoptosis of HepG2 cells. Mechanisms involved may be accumulation of quiescent GO/G1 phase and decrease of Bcl-2 expression. 展开更多
关键词 Liver cancer ns-398 Bcl-2 protein COX-2
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MicroRNA-143 suppresses gastric cancer cell growth and induces apoptosis by targeting COX-2 被引量:15
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作者 Xiao-Li Wu Bin Cheng +5 位作者 Pei-Yuan Li Huan-Jun Huang Qiu Zhao Zi-Li Dan Dean Tian Peng Zhang 《World Journal of Gastroenterology》 SCIE CAS 2013年第43期7758-7765,共8页
AIM:To investigate the function of microRNA-143(miR-143)in gastric cancer and explore the target genes of miR-143.METHODS:A quantitative real-time reverse transcription-polymerase chain reaction(RT-PCR)analysis was pe... AIM:To investigate the function of microRNA-143(miR-143)in gastric cancer and explore the target genes of miR-143.METHODS:A quantitative real-time reverse transcription-polymerase chain reaction(RT-PCR)analysis was performed to evaluate miR-143 expression in gastric cancer cell lines.After transfecting gastric cancer cells with miR-143-5p and miR-143-3p precursors,Alamar blue and apoptosis assays were used to measure the respective proliferation and apoptosis rates.Cyclooxygenase-2(COX-2)expression was determined by realtime RT-PCR and Western blot assays after miR-143transfection.Reporter plasmids were constructed,and a luciferase reporter assay was used to identify the miR-143 binding site on COX-2.RESULTS:Both miR-143-5p and miR-143-3p were significantly downregulated in multiple gastric cancer cell lines.Forced miR-143-5p and miR-143-3p expression in gastric cancer cells produced a profound cytotoxic effect.MiR-145-5p transfection into gastric cancer cells resulted in a greater growth inhibitory effect(61.23%±3.16%vs 46.58%±4.28%,P<0.05 in the MKN-1cell line)and a higher apoptosis rate(28.74%±1.93%vs 22.13%±3.31%,P<0.05 in the MKN-1 cell line)than miR-143-3p transfection.Further analysis indicated that COX-2 expression was potently suppressed by miR-143-5p but not by miR-143-3p.The activity of a luciferase reporter construct that contained the 3’-untranslated region(UTR)of COX-2 was downregulated by miR-143-5p(43.6%±4.86%,P<0.01)but not by miR-143-3p.A mutation in the miR-145-5p binding site completely ablated the regulatory effect on luciferase activity,which suggests that there is a direct miR-145-5p binding site in the 3’-UTR of COX-2.CONCLUSION:Both miR-143-5p and miR-143-3p function as anti-oncomirs in gastric cancer.However,miR-143-5p alone directly targets COX-2,and it exhibits a stronger tumor suppressive effect than miR-143-3p. 展开更多
关键词 gastric cancer MicroRNA-143 Anti-oncomir cyclooxygenase-2 APOPTOSIS
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Helicobacter pylori infection, gastrin and cyclooxygenase-2 in gastric carcinogenesis 被引量:15
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作者 Yun Shao Kun Sun +3 位作者 Wei Xu Xiao-Lin Li Hong Shen Wei-Hao Sun 《World Journal of Gastroenterology》 SCIE CAS 2014年第36期12860-12873,共14页
Gastric cancer is one of the most frequent neoplasms and a main cause of death worldwide, especially in China and Japan. Numerous epidemiological, animal and experimental studies support a positive association between... Gastric cancer is one of the most frequent neoplasms and a main cause of death worldwide, especially in China and Japan. Numerous epidemiological, animal and experimental studies support a positive association between chronic Helicobacter pylori(H. pylori) infection and the development of gastric cancer. However, the exact mechanism whereby H. pylori causes gastric carcinogenesis remains unclear. It has been demonstrated that expression of cyclooxygenase-2(COX-2) is elevated in gastric carcinomas and in their precursor lesions. In this review, we present the latest clinical and experimental evidence showing the role of gastrin and COX-2 in H. pylori-infected patients and their possible association with gastric cancer risk. 展开更多
关键词 Helicobacter pylori GASTRIN cyclooxygenase-2 gastric cancer
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Experimental Studies on Cyclooxygenase-2 Inhibitor Induced Cervical Cancer Hela Cell Apoptosis and Its Molecular Mechanism 被引量:1
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作者 Ling YIN Li-bei WEI Qiu-hong QU Xiao-peng GUO 《Journal of Reproduction and Contraception》 CAS 2007年第4期271-277,共7页
Objective To investigate the Hela cells growth inhibition and apoptosis possible molecular mechanisms. Methods Hela cells were treated with various concentrations (100μmol/L,200μmol/L, 300 μmol/L, 400 μmol/L) of... Objective To investigate the Hela cells growth inhibition and apoptosis possible molecular mechanisms. Methods Hela cells were treated with various concentrations (100μmol/L,200μmol/L, 300 μmol/L, 400 μmol/L) of NS-398 (selective for COX-2 inhibition). Cell growth was measured by MTT (Thiazolyl blue). Apoptosis was detected by double staining flow cytometry (FCM). Levels of PGE: were measured by radioimmunoassay. The expressions of COX-2 protein were also examined by Western blot analysis. Results After treated with different concentrations of NS-398, the growth of Hela cells was suppressed significantly in a dose-and time-dependent manner (P〈0.01). The NS-398 can induce apoptosis with the apoptosis rates at 8.53%-43.46% by FCM in a dose-dependent manner. The release of PGE2 was reduced in Hela cells with the values of 69.26 ± 2.13, 47.46 ± 2.18, 28.15 ± 1.64 and 17.01 ± 1.12, respectively, there was significant difference compared with control group (83.78 ± 1.11) (P〈0.01). The NS-398 could inhibit the activity and expression of COX-2 in a dose- dependent manner and down-regulated the expression of COX-2 protein greatly. Conclusion NS-398 could inhibit the proliferation and increase apoptosis in human Hela cells. These effects may be depended on the inhibition of the expression of COX-2 and PGE2 by NS-398. 展开更多
关键词 cyclooxygenase-2 ns-398 Hela cell APOPTOSIS
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Effect of NS-398 on colon cancer cells
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作者 Xiao-QingJia NingZhong +4 位作者 Li-HuiHan Jing-HuaWang MingYan Fan-LiMeng Shang-ZhongZhang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第3期353-356,共4页
AIM: To study the effect of NS-398, a selective cydooxygenase 2 (COX-2) inhibitor, on invasion of colon cancer cell line HT-29 in vitro and to explore its mechanisms. METHODS: Invasive behaviors of the malignant colon... AIM: To study the effect of NS-398, a selective cydooxygenase 2 (COX-2) inhibitor, on invasion of colon cancer cell line HT-29 in vitro and to explore its mechanisms. METHODS: Invasive behaviors of the malignant colon cancer cell line HT-29 were investigated in this study. Expressions of COX-2 and CD44v6 in HT-29 cells were detected by flow cytometry. Cellular survival rate was determined by MTT assay. The invasive capacity was quantified by a modified Boyden chamber model. Alterations of cytoskeleton component F-actin were observed by confocal laser scanning microscope. RESULTS: Flow cytometry analysis showed that COX-2 was highly expressed in HT-29 cells. The invasive capability of HT-29 cells could be greatly inhibited by NS-398 at the experimental concentrations of 0.1,1.0 and 10 μmol/L with an inhibitory rate of 22.74%, 42.35% and 58.61% (P<0.01), respectively. MTT assay showed that NS-398 at the experimental concentrations had no significant influence on cellular viability, indicating that such anti-invasive effects had no relationship with cytotoxicity. F-actin was mainly distributed around nuclei forming annular structure in HT-29 cells. After exposure to NS-398 of 10 μmol/L, the annular structure around nuclei disappeared and the fluorescence intensity of F-actin decreased obviously. Treatment with NS-398 could down-regulate the expression of CD44v6 as well. CONCLUSION: NS-398 has anti-invasive effects on colon cancer HT-29 cells in vitro, which may be mediated by a novel mechanism of disruption of cytoskeleton. Down-regulation of CD44v6 expression may be related to alterations of cytoskeleton. 展开更多
关键词 Colon cancer ns-398 CYTOSKELETON F-ACTIN COX-2 CD44V6
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NS-398对人胃癌裸鼠移植瘤血管生成的影响 被引量:4
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作者 刘升云 李建生 张金平 《郑州大学学报(医学版)》 CAS 北大核心 2004年第3期418-420,共3页
目的 :探讨NS 398对裸鼠胃癌移植瘤血管生成的影响。方法 :1 2只裸鼠随机分为 2组 ,以人胃癌细胞株SGC790 1建立荷瘤裸鼠动物模型。治疗组于接种第 2d开始给予 1 0mg/kgNS 398腹腔注射 ,隔d给药 ;对照组隔d腹腔注射同体积PBS ,连续 2 0... 目的 :探讨NS 398对裸鼠胃癌移植瘤血管生成的影响。方法 :1 2只裸鼠随机分为 2组 ,以人胃癌细胞株SGC790 1建立荷瘤裸鼠动物模型。治疗组于接种第 2d开始给予 1 0mg/kgNS 398腹腔注射 ,隔d给药 ;对照组隔d腹腔注射同体积PBS ,连续 2 0d ,观察抑瘤率 ,应用免疫组织化学技术检测 2组肿瘤组织环氧合酶 2 (COX 2 )、VEGF表达及微血管密度 (MVD)。结果 :NS 398抑瘤率达 88.7% ,COX 2、VEGF及MVD在治疗组分别为 2 .6± 0 .8,2 .3± 1 .2和 2 1 .2± 4 .8,显著低于对照组的 5 .0± 0 .6 ,5 .8± 0 .4和 4 1 .3± 2 .6 (P均 <0 .0 5 )。结论 :NS 398可能通过抑制COX 2。 展开更多
关键词 血管生成 ns-398 胃癌 环氧合酶2 移植瘤
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丙谷胺和NS-398协同诱导胃癌细胞凋亡的研究 被引量:2
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作者 苏菡 孙为豪 +5 位作者 傅熙玲 邵耘 产松苗 陈国胜 许海尘 朱峰 《医学研究生学报》 CAS 2005年第8期682-685,共4页
目的:探讨胃泌素受体拮抗剂丙谷胺和特异性环氧化酶(COX)-2抑制剂NS-398对人胃腺癌细胞株MKN-45细胞凋亡的调控作用及其机制。方法:MKN-45细胞常规培养于含10%胎牛血清的RPMI1640培养液中,待细胞长至亚单层后加丙谷胺(5mmol/L)和(或)NS-... 目的:探讨胃泌素受体拮抗剂丙谷胺和特异性环氧化酶(COX)-2抑制剂NS-398对人胃腺癌细胞株MKN-45细胞凋亡的调控作用及其机制。方法:MKN-45细胞常规培养于含10%胎牛血清的RPMI1640培养液中,待细胞长至亚单层后加丙谷胺(5mmol/L)和(或)NS-398(0.01mmol/L),连续培养48h。采用流式细胞仪检测细胞凋亡率,RT-PCR法测定凋亡抑制基因bcl-2mRNA表达。结果:丙谷胺组、NS-398组和联合用药组的细胞凋亡率分别为(24.72±3.19)%、(26.69±3.35)%和(36.11±4.57)%,显著高于对照组(1.57±0.55)%(P<0.01),联合用药组的细胞凋亡率明显高于丙谷胺或NS-398单一用药组[(36.11±4.57)%vs(24.72±3.19)%和(26.69±3.35)%,P<0.05]。丙谷胺和NS-398显著下调bcl-2mRNA在MKN-45细胞的表达(P<0.05)。结论:丙谷胺、NS-398通过下调胃癌细胞bcl-2基因表达而诱导细胞凋亡,两者联合使用具有协同作用。 展开更多
关键词 丙谷胺 ns-398 胃癌 细胞凋亡 BCL-2基因
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Effects of combined octreotide and aspirin on the growth of gastric cancer 被引量:5
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作者 唐承薇 王春晖 汤丽平 《Chinese Medical Journal》 SCIE CAS CSCD 2003年第3期54-58,共5页
Objective To investigate the effects of the combination of octreotide and aspirin on the growth of gastric cancer. Methods Proliferation of gastric cancer cell lines treated with octreotide or aspirin was determined b... Objective To investigate the effects of the combination of octreotide and aspirin on the growth of gastric cancer. Methods Proliferation of gastric cancer cell lines treated with octreotide or aspirin was determined by 3 H-thymidine incorporation. After xenografts of human gastric cancer were implanted orthotropically in the stomach of nude mice, they were administered octreotide plus aspirin for 8 weeks. The mRNA of somatostatin receptor in the tissues of gastric carcinoma was detected by reverse transcription polymerase chain reaction (RT-PCR). Cyclooxygenase-2 in gastric cancer tissues was measured by immuno~histochemistry. Results Both octreotide and aspirin significantly reduced the 3 H-thymidine incorporation of gastric cancer cells. Xenografts in situ were found in all stomachs of nude mice except for two in the combination group. Either size or weight of tumors treated by octreotide, aspirin or in combination was significantly reduced as compared with that of controls. The inhibition rate for tumor was 60.6% (octreotide), 39.3% (aspirin), and 85.6% (in combination) respectively. No severe side effects were observed in any treated groups. Somatostatin receptor-2 and -3 were expressed in the transplanted gastric adenocarcinomas. Aspirin could down-regulate the strong expression of cyclooxygenase-2 in the tissue of gastric adenocarcinomas of nude mice.Conclusion A combination of octreotide and aspirin significantly inhibited proliferation of gastric cancer through mediation of somatosatin receptors and suppression of cyclooxygenase-2. 展开更多
关键词 gastric cancer OCTREOTIDE ASPIRIN SOMATOSTATIN cyclooxygenase-2
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