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作 者:陈淑萍[1,2] 陈慧菁[2] 刘枋[1] 叶韵斌[1]
机构地区:[1]福建医科大学研究生教育学院,福州350108 [2]福建省肿瘤医院肿瘤免疫学研究室福建省肿瘤转化医学重点实验室
出 处:《肿瘤研究与临床》2012年第6期361-365,共5页Cancer Research and Clinic
基 金:福建省医学创新课题(2007-CXB-1);国家留学回国人员基金(2007-170)
摘 要:目的分析peptidimer-c对K562细胞基因表达谱的影响,初步探讨peptidimer-c诱导K562细胞凋亡和抑制生长的可能机制。方法应用锥虫蓝染色法计数经不同浓度peptidimer-c分别作用不同时间后的K562活细胞数;通过透射电子显微镜观察peptidimer-c作用前后K562细胞的超微结构;应用HumanU133Plus3.0基因表达谱芯片检测peptidimer-c作用前后K562细胞的差异表达基因;并用反转录聚合酶链反应(RT.PCR)验证芯片结果。结果peptidimer-c能诱导K562细胞凋亡和抑制生长,peptidimer-c作用于K562细胞后引起大量基因表达的变化,差异表达基因有529个,其中上调455个,下调74个,影响细胞凋亡的基因包括JUN、AXUDl、TNFRSFIOB等表达明显上调;RT-PCR验证选取的15个基因的表达差异与芯片结果一致。结论peptidimer-c可通过上调肿瘤坏死因子及其受体家族成员和JUN家族,启动K562细胞凋亡。Objective To analyze the influence of peptidimer-c on the gene expression profiling of K562 cells and investigate the mechanism of peptidimer-e inducing the apoptosis and inhibiting proliferation of K562 cells. Methods Trypan blue staining technique was performed for counting the number of living K562 cells treated with peptidimer-e. The ultrastructure changes of K562 cells treated with peptidimer-c was Observed under transmission electron microscope. The Human U133 Plus 3.0 gene chips were used to detect the differentially expressed genes of K562 cells treated with peptidimer-c. Reverse transcription PCR was conducted to confirm some genes identified by gene chips. Results Peptidimer-c could induce the apoptosis and inhibit the proliferation of K562 cells. Peptidimer-e caused widely changes of the gene expression profiles of K562 cells. The chip data suggested that there were 529 differentially expressed genes, of which 455 genes were up-regulated and 74 genes were down-regulated. The relevant apoptotic genes were down-regulated markedly, including JUN, AXUD1, TNFRSF10B, etc. Fifteen of the differentially expressed genes were detected by RT-PCR, which was consistent with the chip data. Conclusion Peptidimer-c may induce apoptosis of K562 cells by activating the TNF/TNFR family and the JUN family.
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