Transcriptional Regulation of Cyclooxygenase-2 in Mouse Skin Carcinoma Cells

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 investigatedcis- 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.

• Publication year

  1998

• Venue

  Journal of Biological Chemistry

• Publication date

  1998-10-16

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1074/jbc.273.42.27686PMID 9765305
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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