检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:熊莺[1] 孙午[1] 王志[2] 涂艳[1] 刘晓峰[1] 梁皓[2]
机构地区:[1]江西九江市第一人民医院检验科,九江332000 [2]九江市第一人民医院肿瘤科,九江332000
出 处:《中国免疫学杂志》2014年第9期1174-1177,共4页Chinese Journal of Immunology
基 金:江西省卫生厅资助项目(No.20142060)
摘 要:目的:研究肺癌细胞Foxp3、VEGF分泌和TLR2信号通路的关系。方法:使用实时荧光定量RT-PCR检测肺癌细胞A549的TLR2表达情况;使用实时荧光定量RT-PCR和ELISA检测经TLR2激活物肽聚糖处理前后肿瘤Foxp3及VEGF mRNA的水平及其分泌状况;使用实时荧光定量RT-PCR和ELISA检测采取抗TLR2抗体封闭后再用肽聚糖处理前后细胞Foxp3和VEGF mRNA的水平及其分泌状况。结果:肺癌细胞A549上有TLR2的表达;经TLR2激活物肽聚糖处理后肿瘤细胞Foxp3及VEGF mRNA的水平显著增高,在细胞培养上清液中的分泌水平同样显著增加;采用抗TLR2抗体封闭TLR2后,肽聚糖的刺激不会引起肿瘤细胞Foxp3和VEGF mRNA的水平及其分泌水平的增加。结论:TLR2信号通路促进分泌Foxp3和VEGF,参与肺癌细胞免疫逃逸,明确这些对于我们预防诊断和治疗肿瘤有重要意义。Objective: To investigate the relationship between scrected Foxp3, VEGF and TLR2 signaling pathways in lung cancer cells. Methods: TLR2 expression in A549 lung cancer cells were analysed by Real-time fluorescent quantitative PCR. Foxp3 and VEGF mRNA level and its production status were analysed by Real-time fluorescent quantitative PCR and ELISA , which were processed by TLR2 activators peptidoglycan or not in tumor cells. After being closed by anti-TLR2 antibody, Foxp3 and VEGF mRNA level and its production status were analysed by Real-time fluorescent quantitative PCR and ELISA. Results: There were the expression of TLR2 on surface of A549 lung cancer cells. Foxp3 and VEGF mRNA level and the secretion levels are increased significantly in the cell culture supernatant which were processed by TLR2 activators peptidoglycan in tumor cells. After being closed by anti-TLR2 antibody, Foxp3 and VEGF mRNA level did't increase as well as its secretion level. Conclusion: TLR2 signaling pathways are involved in immune escape by promoting the secretion of Foxp3 and VEGF in lung cancer cells, which may play an important role in prevention, diagnose and therapy of tumors
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.118