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

  1. Author:
    Liu, J.
    Malavya, S.
    Wang, X. Q.
    Saavedra, J. E.
    Keefer, L. K.
    Tokar, E.
    Qu, W.
    Waalkes, M. P.
    Shami, P. J.

  2. Author Address

    Liu, Jie, Tokar, Erik, Qu, Wei, Waalkes, Michael P.] NIEHS, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI, Res Triangle Pk, NC 27709 USA. [Malavya, Swati, Shami, Paul J.] Univ Utah, Dept Internal Med, Div Med Oncol, Salt Lake City, UT 84112 USA. [Wang, Xueqian] NIEHS, Pharmacol Lab, Res Triangle Pk, NC 27709 USA. [Saavedra, Joseph E.] SAIC, Basic Sci Program, Frederick, MD USA. [Keefer, Larry K.] NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA.
    1. Year: 2009
  2. Journal: Genomics
    1. 94
    2. 1
    3. Pages: 32-38
  4. Type of Article: Article
  1. 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 THIRS1 and CD36 and genes involved in tumor cell migration such as tissue inhibitors of metal loprotemases, 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. Published by Elsevier Inc.

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  2. DOI: 10.1016/j.ygeno.2009.03.005
  3. PMID: 19348908

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