裸鼠高致瘤性人白血病细胞系肿瘤相关基因的表达

目的：探索K562和K562－n细胞在裸鼠体内致瘤性不同的分子生物学机制。方法：应用基因芯片技术，检测K562细胞和K562－n细胞的差异表达基因。结果：K562－n细胞中表达上调的与白血病及其他肿瘤发生、发展相关的基因包括加dek基因和DP1基因（结肠直肠多发性息肉病位点基因）。许多肿瘤抑制基因或包含潜在的肿瘤抑制基因的序列在K562－n细胞中表达下降，如染色体12p13序列（U47924）.锌指蛋白127－Xp基因和锌指蛋白198基因,prohibitin基因、DNF15s2基因、hMSH2基因（遗传性非息肉性结肠癌基因，为碱基错配修复基因）、环孢素受体基因。结论：K562－n细胞的裸鼠高致瘤特性与一系列癌基因的表达上调和抑癌基因的表达下调有关。

Tumor associated gene expression of human leukemia cell line with high tumorigenicity in nude mice

Objective:To study the molecular tumorigenicity mechanism of K562 and K562-n cell lines in nude mice.Methods:The genes differently expressed in K562 and K562-n cells were detected by using DNA microarray technique, DNA microarray detection were confirmed by hybridization in situ.Results:There were 139 genes differently expressed between K562 and K562-n cells,and among them 85 genes have been registered.There were several oncogenes up-regulated in K562-n cells,such as dek gene and DP1 gene (human polyposis locus).Some tumor suppressor genes or DNA serials with potential tumor suppressor genes,such as zinc-finger protein 127-Xp genes,zinc-finger protein 198 gene,prohibitin gene,DNF15s2 gene,hMSH2 gene(hereditary nonpolyposis colorectal cancer gene),cyclophilin gene and 12p13 serial,were down-regulated in K562-n cells.The results of hybridization in situ coincided with DNA microarray detection.Conclusion:The high tumorigenicity of K562-n cells is related with up-regulation of some oncogenes and down-regulation of some tumor suppressor genes.