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首页> 外文期刊>Genomics >Gene expression profiling for nitric oxide prodrug JS-K to kill HL-60 myeloid leukemia cells.
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Gene expression profiling for nitric oxide prodrug JS-K to kill HL-60 myeloid leukemia cells.

机译：一氧化氮前药JS-K杀死HL-60髓样白血病细胞的基因表达谱。

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摘要

The nitric oxide (NO) prodrug JS-K is shown to have anticancer activity. To profile the molecular events associated with the anticancer effects of JS-K, HL-60 leukemia cells were treated with JS-K and subjected to microarray and real-time RT-PCR analysis. JS-K induced concentration- and time-dependent gene expression changes in HL-60 cells corresponding to the cytolethality effects. The apoptotic genes (caspases, Bax, and TNF-alpha) were induced, and differentiation-related genes (CD14, ITGAM, and VIM) were increased. For acute phase protein genes, some were increased (TP53, JUN) while others were suppressed (c-myc, cyclin E). The expression of anti-angiogenesis genes THBS1 and CD36 and genes involved in tumor cell migration such as tissue inhibitors of metalloproteinases, were also increased by JS-K. Confocal analysis confirmed key gene changes at the protein levels. Thus, multiple molecular events are associated with JS-K effects in killing HL-60, which could be molecular targets for this novel anticancer NO prodrug.
机译：一氧化氮（NO）前药JS-K具有抗癌活性。为了分析与JS-K的抗癌作用相关的分子事件，用JS-K处理HL-60白血病细胞，并对其进行了微阵列和实时RT-PCR分析。 JS-K诱导的HL-60细胞中浓度和时间依赖性基因表达的变化对应于细胞杀伤作用。诱导凋亡基因（胱天蛋白酶，Bax和TNF-α），并增加分化相关基因（CD14，ITGAM和VIM）。对于急性期蛋白基因，一些增加（TP53，JUN），而另一些被抑制（c-myc，cyclin E）。 JS-K也增加了抗血管生成基因THBS1和CD36的表达以及参与肿瘤细胞迁移的基因（例如金属蛋白酶的组织抑制剂）的表达。共聚焦分析证实了蛋白质水平上关键基因的变化。因此，在杀死HL-60中，多种分子事件与JS-K效应有关，后者可能是这种新型抗癌NO前药的分子靶标。

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