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J Biol Chem, Vol. 273, Issue 42, 27686-27694, October 16, 1998
From the Department of Carcinogenesis, University of Texas, M. D. Anderson Cancer Center, Science Park-Research Division,
Smithville, Texas 78957
Many studies have suggested that overexpression
of cyclooxygenase-2 (COX-2) contributes to the development of tumors in
several tissues. COX-2 expression tends to be up-regulated in various types of tumors and transformed cell lines, and the overexpression of
COX-2 is caused by enhanced transcription of the gene. In an attempt to
characterize the signaling pathway leading to the overexpression of
COX-2 in the mouse skin carcinoma cell line JWF2, we investigated cis- and trans-acting factors required for
COX-2 expression and demonstrated a molecular mechanism by which COX-2
is expressed differentially in normal and neoplastic tissues. Two
regions of the COX-2 promoter containing an E-box and nuclear factor
IL6 site were identified as the positive regulatory elements through transient transfections with luciferase reporter vectors containing the
various 5'-flanking regions of the promoter. Moreover, electrophoretic mobility shift assays and cotransfection experiments showed that upstream stimulatory factors and CCAAT/enhancer-binding proteins (C/EBPs) bind to the E-box and nuclear factor IL6 site, respectively, and functionally transactivate the COX-2 promoter. We also found that
C/EBP isoforms are expressed differentially during mouse skin
carcinogenesis, suggesting that overexpression of COX-2 in tumors may
be caused by a change in C/EBP expression levels.
Transcriptional Regulation of Cyclooxygenase-2 in Mouse Skin
Carcinoma Cells
REGULATORY ROLE OF CCAAT/ENHANCER-BINDING PROTEINS IN THE
DIFFERENTIAL EXPRESSION OF CYCLOOXYGENASE-2 IN NORMAL AND NEOPLASTIC
TISSUES
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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