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作 者:杨光[1] 张放[1] 江弢[1] 黄克俭[1] 曹俊[1] 黄陈[1] 裘正军[1]
机构地区:[1]上海交通大学附属第一人民医院普外科,上海200080
出 处:《中华胰腺病杂志》2009年第1期48-50,共3页Chinese Journal of Pancreatology
摘 要:目的探讨IL-6对人胰腺癌细胞株Capan-2生长及STAT3信号转导途径的影响。方法采用MTr法检测不同浓度IL-6刺激后Capan-2细胞的增殖率;免疫细胞化学染色确定磷酸化STAT3(P.STAT3)在Capan-2细胞内的定位及IL-6刺激前后表达量的变化;流式细胞仪检测细胞的凋亡;Westernblot检测IL-6刺激前后Capan-2细胞中P—STAT3、bcl—xl、Cyclin D1蛋白表达量的变化。结果100ng/ml的IL-6作用Capan.2细胞后,细胞的增殖从1增加到4.965-t-0.18(P〈0.05);细胞凋亡率从(3.21±0.23)%下降到(1.98±0.67)%(P〈0.05);P-STAT3、bcl-xl、Cyclin D1蛋白表达明显升高(P〈0.05),且bcl-xl的表达与P—STAT3的表达呈正相关(r=0.985,P=0.015);CyclinD1的表达与P-STAT3表达也呈正相关(r=0.914,P=0.036)。结论JAK/STAT信号转导途径的活化介导了IL-6对Capan-2细胞的增殖促进功能。Objective To investigate the effect of interleukin 6 (IL-6) on the growth and proliferation of human pancreatic cancer cell line Capan-2 and the signal transduction pathway. Methods MTT method was used to detect the effect of IL-6 of different concentrations on the growth and proliferation of Capan - 2 ceils ; cell apoptosis was detected by flow cytometry; the intracellular localization of phosphorylated STAT3 ( PSTAT3) was determined by immunocytocbemistry and western blot were used to detect P-STAT3, bcl-xl and Cyclin D1 in Capan-2 cells stimulated by IL-6. Results IL-6 (100 ng/ml) could remarkably promote the growth of Capan-2 cells from 1 to 4. 965 ± 0. 18 ( P 〈 0. 05 ) ; the percentage of apoptosis decreased significantly from (3.21 ± 0.23 ) % to ( 1.98 ±0.67 ) % ( P 〈 0.05 ) ; the expressions of P-STAT3, bel-xl, Cyclin D1 increased significantly ( P 〈 0.05 ) , and the expressions of bcl-xl was positively correlated with that of P-STAT3 (r = 0. 985, P = 0. 015 ) ; the expressions of Cyclin D1 was also positively correlated with that of P- STAT3 (r = 0.914, P = 0. 036). Conclusions IL-6 activated JAK/STAT signal transduction pathway, which played an important role in the growth and proliferation of Capan-2 cells in the presence of IL-6.
关 键 词:胰腺肿瘤 白细胞介素6 信号转导及转录活化因子3
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