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Aim To investigate the apoptosis of human gastric carcinoma AGS cells induced by cecropinXJ. Methods Human gastric carcinoma AGS cells and human normal epithelial cells GES-1 were co-cultured with different concentrations of cecropinXJ ranging from 0. 01 to 1 000 mg·L-1 for 24 h. MTT assay was used to observe the effects of cecropinXJ on the proliferation of AGS cells and GES-1 cells. The ultrastructural changes of the AGS cells were observed by transmission electron microscopy. Hoechst staining was used to de-tect cell apoptosis. The changes of intracellular reac-tive oxygen species ( ROS) and mitochondrial potential were analysed by flow cytometery. The expression of Bax, Bcl-2, caspase-3 and cytochrome C in mRNA level was investigated by qRT-PCR. Western blot was used to determine the protein expression of Bax, Bcl-2, caspase-3 and cytochrome C. Results CecropinXJ significantly suppressed the proliferation of AGS cells in vitro (P<0. 05) in a dose-dependent manner, IC50 =61. 19 mg·L-1 , but had no inhibitive effects on the proliferation of GES-1 cells. After treatment for 24 h, cecropinXJ induced AGS cells nuclear condensation, and increased ROS production, disrupted mitochondri-al integrity. The results of qRT-PCR and Western blot demonstrated cecropinXJ could up-regulate the expres-sion of Bax and down-regulate the expression of Bcl-2 , promote the release of cytochrome C and activate caspase-3. Meanwhile, cecropinXJ promoted caspase-3 activity in a dose-dependent manner, and cell death ratio of AGS cells induced by cecropinXJ was signifi-cantly reduced by caspase-3 and caspase-9 specific in-hibitors treatment. Conclusion CecropinXJ can in-duce apoptosis of AGS cells by downregulating Bcl-2 , upregulating Bax and activating caspase-3 , which may be one of its anti-tumor mechanisms.
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EBV infection has been causally associated with incidence of many carcinomas. EBV-associated gastric carcinoma (EBVaGC) has been classified as a unique gastric carcinoma subset, suggesting EBV infection is related to the development of gastric cancer. In this study, general trends of EBVaGC studies for last half-decades were reviewed in several perspectives of clinical significance, virological importance and etiological interests. Throughout this comprehensive reviewing, new study trends of EBV and EBVaGC for next half-decades were suggested.
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Infecções por Vírus Epstein-Barr , Herpesvirus Humano 4 , Incidência , Metilação , Prognóstico , Neoplasias GástricasRESUMO
OBJECTIVE: To investigate aticancer effect and potential mechanism of a new xanthono-pyridine derivative N, N'-(7-oxo-7H-chromenoquinoline-5, 9-diyl)-bis(2-(pyrrolidin-1-yl)acetamide) (XP-16) on human gastric carcinoma cell line MGC-803.
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This article was aimed to investigate the cell proliferation , cell apoptosis and its related molecular mechanisms of the human gastric carcinoma cell line BGC-823 in v itro after treatment with cinnamaldehyde . The MTT Assay demonstrated the inhibitory effect of cinnamaldehyde . And the Flow Cytometry was used to determine its induction of cell apoptosis. The Hoechst 33342 was used to observe morphological changes during apoptosis . Moreover , quantitative real time PCR and western blot analysis were used to detect the effect of cinnamaldehyde on human gastric carcinoma cell line BGC-823 . The results showed that compared with the control group , cinnamaldehyde had inhibitory effect on human gastric carcinoma cell line BGC-823 ( P <0 . 01 ) . It showed that cinnamaldehyde induced apoptosis through the downregulation of Bcl-2 , Bcl-xL and Survivin expression , upregulation of Bax and Bak expression , downregulation of Bcl-2 and Procaspase-3 , and upregulation of BAX . It was concluded that cinnamaldehyde had inhibitory effect on the proliferation of human gastric carcinoma cell line BGC-823 and induced apoptosis . It may be related to the activation of the endogenous apoptosis pathway .
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The aim of this study was to investigate the effect of Paris saponin Ⅰ (PS Ⅰ ) on human gastric carcinoma cell growth and apoptosis and to explore the potential mechanisms.The proliferation of SGC7901 cells was monitored by the MTT cell viability assay,while the nuclear morphology of apoptotic cells was assessed by Hoechst 33258 staining.Flow cytometry was performed to analyze the cell cycle progression of propidium iodide (PI)-stained SGC7901 cells and the apoptotic rate of annexin V/PI-stained cells.Western blotting was used to examine the expression of several cell cycle proteins,including cyclin B1 and Cdkl,and the apoptosis-regulated proteins Bcl-2,Bax,cytochrome c,procaspase-9,and procaspase-3.The MTT assay demonstrated that PSⅠ could induce significant doseand time-dependent inhibition of SGC7901 cell proliferation.Marked morphological changes,including condensation of chromatin,nuclear fragmentation and apoptotic bodies were clearly shown on Hoechst 33258 staining.PSⅠ treatment also resulted in the disruption of the cell cycle at G2/M and the induction of apoptosis.Following PSⅠ treatment,the cell cycle-related proteins cyclin B 1 and Cdk1 were downregulated.Expression of the pro-apoptotic protein Bax was increased,while anti-apoptotic protein Bcl-2decreased.PSⅠ treatment resulted in elevated cytoplasmic cytochrome c and activation of the apoptotic proteases caspase-9 and caspase-3.These data indicate that PSⅠ acts as an inhibitor of proliferation in SGC7901 cells by inducing cell cycle arrest and mitochondria-dependent apoptosis.PSⅠ is a potential therapeutic agent against human gastric carcinoma.
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To explore the effects of Taushinone ⅡA on the proliferation, apoptosis and gene ex- pression of p53 and bcl-2 in human gastric carcinoma MKN-45 cells. Cell count and MTT assay were used to study the proliferation-inhibiting effect of Tanshinone ⅡA on MKN-45 cells. The effect of Tanshinone ⅡA on the cell cycle and apoptosis of MKN-45 cells were examined by propidium io- dide (PI) staining and flow cytometry. Semi-quantitative RT-PCR was used to further verify the ex- pression of p53 and bcl-2 gene after exposure to Tanshinone ⅡA in MKN-45 cells. The results showed that Tanshinone ⅡA significantly inhibited the growth and proliferation of MKN-45 cells in a dose- and time-dependent manner (P<0.05). Tanshinone ⅡA arrested MKN-45 cells in G2/M phase which led to an obvious accumulation of G2/M phase cells while decreased number of G0/G1 phase cells. This resulted in apoptosis of MKN-45 cells and the apoptosis rate was as high as 43.91% after treatment with 2.0 μg/mL Tanshinone ⅡA for 96 h. It was also found that Tanshinone ⅡA up-regulated expression of p53 gene and down-regulated expression of bcl-2 gene. The cytostatic and antiproliferative effect of Tanshinone ⅡA makes it a promising anticancer agent for the treatment of gastric carcinoma.
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PURPOSE: Oxaliplatin (LOHP), 5-FU, and paclitaxel (PTX) are considered highly active against advanced gastric carcinomas, and the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, ZD1839 is considered as a good candidate for the treatment of gastric cancers when given alone or in combination with cytotoxic agents. The present study evaluated the antitumor effects of these agents in SNU-1 human gastric cancer cells either alone or when given as a doublet (i.e., as a cytotoxic-cytostatic combination). MATERIALS AND METHODS: We selected SNU-1 cells that showed DNA mismatch repair (MMR) deficiency and EGFR overexpression. Growth inhibition was measured by MTT and by direct cell counting and cell cycle distribution by flow cytometry. The combination index (CI) was used to describe synergistic interaction. RESULTS: The four drugs showed IC50s ranging from 1.81 nM to 13.2microM. MTT assay appeared to underestimate the cytotoxicity of PTX, which was attributed to a significant resistant fraction (32%). LOHP and PTX induced G2/M arrest, 5-FU increased in S phase, and ZD1839 in-creased in G1 in a concentration dependent manner. PTX ZD1839 showed the greatest synergism and LOHP ZD1839 showed a similar result. The cell cycle effect of PTX was potentiated by the coadministration of ZD1839. A previously developed cytostatic TPi model was used to assess the contribution of cell cycle arrest to overall growth inhibition, and 64% and 80% of the overall growth inhibition was attributed to cell cycle arrest for LOHP and PTX, when exposed to 7.55microM and 10 nM for 72 hr, respectively. CONCLUSION: This study demonstrates the antitumor activity and significant cell cycle arrest effect of ZD1839 against human gastric carcinoma cells and its synergistic interaction with LOHP and PTX. These results provide a preclinical rationale for the clinical development of ZD1839 and its use in combination with LOHP or PTX against human gastric cancers that express EGFR.
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Humanos , Contagem de Células , Ciclo Celular , Pontos de Checagem do Ciclo Celular , Citotoxinas , Reparo de Erro de Pareamento de DNA , Citometria de Fluxo , Fluoruracila , Concentração Inibidora 50 , Paclitaxel , Proteínas Tirosina Quinases , Receptores ErbB , Robenidina , Fase S , Neoplasias GástricasRESUMO
OBJECTIVE:To detect the expressions of five gastric cancer cell metastasis associated genes induced by arsenic trioxide METHODS:The expressions of CD44,P53,nm23,H-ras,PCNA induced by arsenic trioxide were examined by immunohistochemistry method RESULTS:Arsenic trioxide induced the decrease of the expressions of CD44,P53,PCNA in gastric cancer cells;the expressions of nm23 and H-ras were not changed by As2 O 3 CONCLUSION:It is tentatively proved that the antineoplastic action of As2 O 3 may be related to the down-regulation of CD44,P53 and PCNA
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AIM To study the effects of vitamin E succinate (VES) on the cell growth and the DNA synthesis of human gastric carcinoma cell (SGC 7901). METHODS The growth curve was determined with counting viable cell numbers. The colony formations were counted with Giemsa dye staining. The cell cycle was analyzed using flow cytometry (FCM) and the DNA synthesis was observed with the 3H TdR incorporation method. RESULTS VES could inhibit the growth and colony formation of SGC 7901 cells. Growth curve display:after SGC 7901 cells were treated with 5 mg?L -1 、10 mg?L -1 and 20 mg?L -1 VES for seven days, the inhibition rate are 41 2%、98 3% and 100%, respectively. The colony formation of SGC 7901 cell at 24 h was inhibited 6 7%、50 4%、87 2%, and at 48 h was 24 7%、73 4%、100%, respectively. FCM analysis revealed that VES could decrease the percentage of cells in G 2 M phase after treated 48 h in a dose dependent manner, while increase the percentage of cells in S pheise. The assays of 3H TdR incorporation into DNA showed obvious inhibition dose dependently after exposure to VES for 48 h. CONCLUSION VES could inhibit gastric carcinoma cell growth by arresting DNA synthesis in vitro .
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Actinomycin 23-21 ( ACT 23-21 ) is an anticancer antibiotic of Actinmycines. This antibiotic was produced from soil Streptomyces flaveolus which was isolated and obtained from soil samples in Fuzhou, China.The effects of ACT 23-21 were observed on using 2 transplanted models of human nasophryangeal carcinomatous cells ( CNE-2Z ) and human gastric carcinomatous cells ( MGc-803 ) in nude mice. At ACT 23-21 50?g/kg, the inhibition rate for transplanted tumors of CNE-2Z and MGc-803 were 58.4% (P
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Objective:To construct specific small interfering RNA(siRNA) expressing vectors of intracellular Ca2+ transport protein(CaT1)gene and detect its silencing effects.Methods:The hairpin sequences of siRNAs targeting CaT1 gene were designed,synthesized and cloned into pSlincer 3.1-H1 plasmids after annealing.The vectors were then enriched in E.coli.The recombinant pSlincer 3.1-H1 plasmids were identified by restriction endonuclease cutting and DNA sequencing and then transfected into Human Gastric Carcinoma Cell Line BGC-823.The expression of CaT1 mRNA was examined by RT-PCR.Results:The siRNA oligonucleotides of CaT1 were correctly cloned into the pSlincer 3.1-H1 plasmids and confirmed by restriction endonuclease cutting and DNA sequencing.RT-PCR analysis revealed that the expression of CaT1 mRNA in BGC-823 cells transfected with the pSlincer 3.1-H1 constructs of siRNA was significantly decreased compared with that of the negative control and untransfected group.Conclusion:siRNA expression plasmids for silencing Ca2+ transport protein gene are successfully constructed,and they effectively inhibit the CaT1 gene expression.
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Objective To explore the effect of phytic acid on apoptosis of human gastric carcinoma SGC-7901 cells and its mechanism. Method The inhibiting action of phytic acid on SGC-7901 cells was examined by MTT assay; the morphology alteration of SGC-7901 cells was examined by reverse discrepancy microscope; and the expression of c-myc protein was detected by immunohistochemisty method and Western blot method. Results Phytic acid inhibited the growth of human gastric carcinoma SGC-7901 cells in dose and time dependent manner. The growth of cells in test groups were inhibited higher than in control group. The expression of c-myc protein in phytic acid group was lower compared with control group,and reduced in a dose-dependent manner. Conclusion Phytic acid can induce apoptosis of human gastric carcinoma SGC-7901 cells,and the mechanism may be related to apoptosis associated gene c-myc.