本文研究青钱柳多糖(polysaccharides isolated from Cyclocarya paliurus(Batal.)Iljinskjk,PCP)对人胃癌MGC_803细胞生长的影响。采用噻唑蓝(MTT)法检测PCP对MGC_803细胞生长的影响;Annexin法检测PCP对MGC803细胞诱导凋亡的作用。实...本文研究青钱柳多糖(polysaccharides isolated from Cyclocarya paliurus(Batal.)Iljinskjk,PCP)对人胃癌MGC_803细胞生长的影响。采用噻唑蓝(MTT)法检测PCP对MGC_803细胞生长的影响;Annexin法检测PCP对MGC803细胞诱导凋亡的作用。实验结果表明PCP在50、100、200、400μg/mL浓度条件下,均可极显著性抑制人胃癌MGC_803细胞生长(P<0.01),抑制率可达65.07%,细胞凋亡率可达25.44%。说明青钱柳多糖具有抑制人胃癌MGC803细胞生长的生物活性。展开更多
AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated...AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated MGC-803 cells were treated with 5, 10, 20, 40, and 60 μmol/L PBA for 1-4 d. Cell proliferation was detected using the MTT colorimetric assay. Cell cycle distributions were examined using flow cytometry.RESULTS: The proliferation of gastric carcinoma cells was inhibited by PBA in a doseand time-dependent fashion. Flow cytometry showed that SGC-7901 cells treated with low concentrations of PBA were arrested at the G0/G1 phase, whereas cells treated with high concentrations of PBA were arrested at the G2/M phase. Although MGC-803 cells treated with low concentrations of PBA were also arrested at the G0/G1 phase, cells treated with high concentrations of PBA were arrested at the S phase. CONCLUSION: The growth inhibitory effect of PBA on gastric cancer cells is associated with alteration of the cell cycle. For moderately-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and G2/M phases. For lowly-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and S phases.展开更多
Objective: To investigate the effect of activation of peroxisome proliferator-activated receptor gamma (PPARy) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods: The inhibitory of pioglitazone (...Objective: To investigate the effect of activation of peroxisome proliferator-activated receptor gamma (PPARy) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods: The inhibitory of pioglitazone (PGZ) on proliferation of MGC803 cells was analyzed by MTT assay. Cell cycle was detected by flow cytometry (FCM). The expressions of PPARy, cyclin D1 and cell cycle protein-dependent kinase CDK4 in MGC803 cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Treatment with 0.1-10 μmol/L PGZ for 96 h significantly inhibited cell proliferation. The proportion of MGC803 cells at G1 phase was significantly increased when treated with 10 μmol/L PGZ for 48, 72 and 96 h, and showed an apparent G1 phase arrest. The expression of PPARy was at a low level in MGC803 cells and significantly up-regulated when treated with 10 μmol/L PGZ for 48 h (P〈0.01). The expression of CDK4 in MGC803 cells was remarkably down-regulated when treated with 10 μmol/L PGZ for 48 h and the expression of cyclin D1 was slightly down-regulated (P 〈 0.01). Conclusion: Activation of PPARy significantly induced G1 phase arrest, which was associated with down-regulation of the expressions of CDK4 and cyclin DI.展开更多
文摘本文研究青钱柳多糖(polysaccharides isolated from Cyclocarya paliurus(Batal.)Iljinskjk,PCP)对人胃癌MGC_803细胞生长的影响。采用噻唑蓝(MTT)法检测PCP对MGC_803细胞生长的影响;Annexin法检测PCP对MGC803细胞诱导凋亡的作用。实验结果表明PCP在50、100、200、400μg/mL浓度条件下,均可极显著性抑制人胃癌MGC_803细胞生长(P<0.01),抑制率可达65.07%,细胞凋亡率可达25.44%。说明青钱柳多糖具有抑制人胃癌MGC803细胞生长的生物活性。
基金Supported by Natural Science Foundation of Ningbo, No. 2009A610134Natural Sciences Foundation of Zhejiang, No. Y207244+3 种基金College Students’ Science-Technology Innovation Program of Zhejiang Province, No. 200959the Excellent Disser-tation Foundation of Ningbo University, No. 201014KC Wong Magna Fund of Ningbo Universitythe Scientific Innovation Team Project of Ningbo, No.2011B82014
文摘AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated MGC-803 cells were treated with 5, 10, 20, 40, and 60 μmol/L PBA for 1-4 d. Cell proliferation was detected using the MTT colorimetric assay. Cell cycle distributions were examined using flow cytometry.RESULTS: The proliferation of gastric carcinoma cells was inhibited by PBA in a doseand time-dependent fashion. Flow cytometry showed that SGC-7901 cells treated with low concentrations of PBA were arrested at the G0/G1 phase, whereas cells treated with high concentrations of PBA were arrested at the G2/M phase. Although MGC-803 cells treated with low concentrations of PBA were also arrested at the G0/G1 phase, cells treated with high concentrations of PBA were arrested at the S phase. CONCLUSION: The growth inhibitory effect of PBA on gastric cancer cells is associated with alteration of the cell cycle. For moderately-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and G2/M phases. For lowly-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and S phases.
文摘Objective: To investigate the effect of activation of peroxisome proliferator-activated receptor gamma (PPARy) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods: The inhibitory of pioglitazone (PGZ) on proliferation of MGC803 cells was analyzed by MTT assay. Cell cycle was detected by flow cytometry (FCM). The expressions of PPARy, cyclin D1 and cell cycle protein-dependent kinase CDK4 in MGC803 cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Treatment with 0.1-10 μmol/L PGZ for 96 h significantly inhibited cell proliferation. The proportion of MGC803 cells at G1 phase was significantly increased when treated with 10 μmol/L PGZ for 48, 72 and 96 h, and showed an apparent G1 phase arrest. The expression of PPARy was at a low level in MGC803 cells and significantly up-regulated when treated with 10 μmol/L PGZ for 48 h (P〈0.01). The expression of CDK4 in MGC803 cells was remarkably down-regulated when treated with 10 μmol/L PGZ for 48 h and the expression of cyclin D1 was slightly down-regulated (P 〈 0.01). Conclusion: Activation of PPARy significantly induced G1 phase arrest, which was associated with down-regulation of the expressions of CDK4 and cyclin DI.