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*
Department of Biochemistry and Molecular Biology, University of Illinois, Chicago, IL 60612; and
University of California, San Francisco Diabetes Center, Metabolic Research Unit/Hormone Research Institute, University of California, San Francisco, CA 94143
We have previously shown that exposure of P815 tumor cells to
melphalan (L-phenylalanine mustard;
L-PAM) leads to up-regulation of B7-1 surface
expression, and this L-PAM-induced up-regulation requires
de novo RNA synthesis and is associated with accumulation of B7-1 mRNA.
Here we show that the effect of L-PAM on B7-1 surface
expression can be mimicked by exposing P815 tumor cells to oxidative
stress but not to heat shock. Moreover, the antioxidant
N-acetyl-L-cysteine prevented the
L-PAM-induced accumulation of B7-1 mRNA in P815 tumor
cells, suggesting that reactive oxygen species are involved in the
transcriptional regulation of L-PAM-induced B7-1 gene
expression. Although AP-1 and NF-
B are regarded as redox-sensitive
transcription factors and the promoter/enhancer region of the B7-1 gene
contains an AP-1 and an NF-B binding site, exposure of P815 tumor
cells to L-PAM led to rapid and transient activation only
of NF-B, but not AP-1, that bound specifically to a probe containing
the respective binding site in the murine or human B7-1 gene. Moreover,
exposure of P815 tumor cells to a cell-permeable peptide that
selectively inhibits NF-B activation by blocking the activation of
the IB-kinase complex was found to inhibit the
L-PAM-induced B7-1 mRNA accumulation, indicating that
NF-B activation is essential for the L-PAM-induced B7-1
gene expression. Taken together, these results indicate that
L-PAM leads to activation of B7-1 gene expression by
activating NF-B via a pathway that involves reactive oxygen
species.
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