Objective:To detect the expression of RECK gene in the highly and low metastatic cell sublines of human osteosarcoma cell HOS and explore its possible roles on the occurrence and metastasis of osteosarcoma.Methods:RT-...Objective:To detect the expression of RECK gene in the highly and low metastatic cell sublines of human osteosarcoma cell HOS and explore its possible roles on the occurrence and metastasis of osteosarcoma.Methods:RT-PCR, gelatin zymography, and matrigel invasion assay were respectively used to evaluate the endogenous expression of RECK mRNA, MMP-2 activation ratio and invasive capacity in the two osteosarcoma cell sublines.Results:The highly metastatic cell group expressed significantly lower mRNA level of RECK than the low metastatic cell group(P < 0.05), but showed higher MMP-2 activation ratio and invasive capacity(P < 0.05 and P < 0.01, respectively).Conclusion:The abnormal low expression of RECK may participate in osteosarcoma invasion and metastasis, and may be a new therapeutic target for osteosarcoma.展开更多
AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation...AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation of SGC-7901 cells.Apopt osis-inducing effect was determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling with Hoechst staining.Expression of mRNA and protein in Bcl-2 and Bax was analyzed by reverse transcription-polymerase chain reaction and Western blot.Antitumor effect of acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS:Forty-eight hours after treatment with acetylshikonin,MTT assay showed that acetylshikonin inhibited the proliferation of SGC-7901 cells in a dose-dependent manner.The half maximal inhibitory concentration of acetylshikonin to SGC-7901 cells was 0.428±0.07 mg/L.Cell shrinkage,nuclear pyknosis and chromatin condensation,which are the characteristics of cell apoptosis,were observed in treated SGC-7901 cells and the percentage of apoptosis increased in a dose-dependent manner.Acetylshikonin downregulated the expression of Bcl-2 and up-regulated the expression of Bax in the treated SGC-7901 cells compared with the controls.The experiment in vivo showed that 0.5,1,and 2 mg/kg of acetylshikonin significantly inhibited the growth of tumor in the mouse SGC-7901 model,with an inhibitory rate of 25.00%-55.76%. CONCLUSION:Acetylshikonin inhibits the growth of SGC-7901 cells in vitro and in vivo by inducing cell apoptosis.展开更多
文摘Objective:To detect the expression of RECK gene in the highly and low metastatic cell sublines of human osteosarcoma cell HOS and explore its possible roles on the occurrence and metastasis of osteosarcoma.Methods:RT-PCR, gelatin zymography, and matrigel invasion assay were respectively used to evaluate the endogenous expression of RECK mRNA, MMP-2 activation ratio and invasive capacity in the two osteosarcoma cell sublines.Results:The highly metastatic cell group expressed significantly lower mRNA level of RECK than the low metastatic cell group(P < 0.05), but showed higher MMP-2 activation ratio and invasive capacity(P < 0.05 and P < 0.01, respectively).Conclusion:The abnormal low expression of RECK may participate in osteosarcoma invasion and metastasis, and may be a new therapeutic target for osteosarcoma.
文摘AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation of SGC-7901 cells.Apopt osis-inducing effect was determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling with Hoechst staining.Expression of mRNA and protein in Bcl-2 and Bax was analyzed by reverse transcription-polymerase chain reaction and Western blot.Antitumor effect of acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS:Forty-eight hours after treatment with acetylshikonin,MTT assay showed that acetylshikonin inhibited the proliferation of SGC-7901 cells in a dose-dependent manner.The half maximal inhibitory concentration of acetylshikonin to SGC-7901 cells was 0.428±0.07 mg/L.Cell shrinkage,nuclear pyknosis and chromatin condensation,which are the characteristics of cell apoptosis,were observed in treated SGC-7901 cells and the percentage of apoptosis increased in a dose-dependent manner.Acetylshikonin downregulated the expression of Bcl-2 and up-regulated the expression of Bax in the treated SGC-7901 cells compared with the controls.The experiment in vivo showed that 0.5,1,and 2 mg/kg of acetylshikonin significantly inhibited the growth of tumor in the mouse SGC-7901 model,with an inhibitory rate of 25.00%-55.76%. CONCLUSION:Acetylshikonin inhibits the growth of SGC-7901 cells in vitro and in vivo by inducing cell apoptosis.
