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Priming Up-Regulates IFN-Stimulated Gene Factor 3 (ISGF3) Components, Augmenting Responsiveness of IFN-Resistant Melanoma Cells to Type I IFNs
Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia
IFN-stimulated gene factor 3 (ISGF3) mediates transcriptional
activation of IFN-sensitive genes (ISGs). The component subunits of
ISGF3, STAT1
ß, STAT2, and p48-ISGF3
, are tyrosine
phosphorylated before their assembly into a complex. Subsequently, the
ISGF3 complex is translocated to the nucleus. We have recently
established that the responsiveness of human melanoma cell lines to
type I IFNs correlates directly with their intracellular levels of
ISGF3 components, particularly STAT1. In the present study, we show
that pretreating IFN-resistant melanoma cell lines with IFN-
(IFN- priming) before stimulation with type I IFN also results in
increased levels of ISGF3 components and enhanced DNA-binding
activation of ISGF3. In addition, IFN- priming of IFN-resistant
melanoma cell lines increased expression of type I IFN-induced ISG
products, including ISG54, 2'-5'-oligoadenylate synthase, HLA class I,
B7-1, and ICAM-1 Ags. Furthermore, IFN- priming enhanced the
antiviral effect of IFN-ß on the IFN-resistant melanoma cell line,
MM96. These results support a role for IFN- priming in up-regulating
ISGF3, thereby augmenting the responsiveness of IFN-resistant melanoma
cell lines to type I IFN and providing a molecular basis and
justification for using sequential IFN therapy, as proposed by others,
to enhance the use of IFNs in the treatment of melanoma.
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