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目的:研究探讨5-氨基乙酰丙酸介导的光动力疗法(ALA-PDT)对白血病细胞株HL-60的作用机制。方法:以白血病细胞株HL-60为实验模型。实验分为2组,对照组(未处理组)及ALA+PDT组。利用人全基因组基因表达谱芯片技术研究ALA-PDT后HL-60细胞基因改变情况。结果:人全基因组芯片共检测了48 000个基因,用RT-PCR的方法验证了数据的可靠性,对芯片结果产生的数据分析发现:ALA-PDT影响了细胞的多种生命进程,如转录调控,抑制翻译过程;促进一系列应激反应;上调促凋亡基因的表达,抑制抗凋亡基因的表达,促进凋亡的发生。结论:ALA-PDT通过诱导凋亡的方式杀伤HL-60细胞。多种调控机制参与凋亡的发生:c-Abl和PML基因是上调基因网络中的主导基因,共同参与了凋亡的发生。线粒体途径和TNF途径激活,DEDD2及CDC2L2介导的凋亡通路也占了一定的地位。ERN1、Bcl2、及c-Jun等基因参与其中促进凋亡的发生。
AIM: To investigate the mechanism of 5-aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) on leukemia cell line HL-60. Methods: leukemia cell line HL-60 as experimental model. The experiment was divided into two groups, control group (untreated group) and ALA + PDT group. Human genome-wide cDNA microarray was used to study the genetic alteration of HL-60 cells after ALA-PDT. Results: 48 000 genes were detected in human whole genome chip, and the reliability of the data was verified by RT-PCR. The data analysis of the chip results showed that ALA-PDT affected various cell life processes such as transcription Regulate and inhibit the translation process; promote a series of stress response; up-regulate the expression of pro-apoptotic genes, inhibit the expression of anti-apoptotic genes and promote apoptosis. Conclusion: ALA-PDT can kill HL-60 cells by inducing apoptosis. A variety of regulatory mechanisms involved in the occurrence of apoptosis: c-Abl and PML genes are up-regulated genes in the network of genes involved in the occurrence of apoptosis. Mitochondrial pathway and TNF pathway activation, DEDD2 and CDC2L2-mediated apoptosis pathway also accounted for a certain status. ERN1, Bcl2, and c-Jun and other genes involved in the promotion of apoptosis.