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    Genomics. 2009 Jul;94(1):32-8. Epub 2009 Apr 5.

    Gene expression profiling for nitric oxide prodrug JS-K to kill HL-60 myeloid leukemia cells.

    Liu J, Malavya S, Wang X, Saavedra JE, Keefer LK, Tokar E, Qu W, Waalkes MP, Shami PJ.

    Source

    Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, National Cancer Institute at NIEHS, Research Triangle Park, NC, USA. Liu6@niehs.nih.gov

    Abstract

    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.

    PMID:
    19348908
    [PubMed - indexed for MEDLINE]

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