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• W2324729880 abstract "Cyclooxygenase-2 (COX-2) is selectively overexpressed in colorectal tumours. The mechanism of COX-2 induction is not fully understood, but requires de novo messenger RNA and protein synthesis, indicating regulation at the transcriptional level. Sequence analysis of the 5′-flanking region of the COX-2 gene shows two nuclear factor-κB (NF-κB) sites. Inhibition of this protein in model cell culture systems attenuates COX-2 expression and implies that NF-κB plays an important role in COX-2 induction. We measured COX-2, NF-κB and IκB kinase α (IKKα) protein expression in matched colonic biopsy samples comprising both nontumour and adjacent tumour tissue from 32 colorectal cancer patients using immunohistochemistry. There was none or very little expression of COX-2, NF-κB and IKKα in non-neoplastic colon epithelial cells, while the expression of all three of these proteins was significantly increased (P<0.05, Wilcoxon's signed rank test) in adjacent cancerous cells. Moreover, all three proteins were found to be coexpressed in the neoplastic epithelium, with the expression of COX-2 and NF-κB highly correlated (Pearson's correlation, P<0.005). There was no apparent correlation between enhanced COX-2, NF-κB or IKKα expression and tumour Dukes' stages. Our results are compatible with the hypothesis that IKKα and NF-κB are involved in COX-2 induction in these tumours and the lack of association between COX-2 expression and severity of disease as measured by Dukes' stage is consistent with the proposal that COX-2 expression is an early postinitiation event." @default.
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• W2324729880 date "2003-05-01" @default.
• W2324729880 modified "2023-10-15" @default.
• W2324729880 title "Upregulation of cyclooxygenase-2 is accompanied by increased expression of nuclear factor-κB and IκB kinase-α in human colorectal cancer epithelial cells" @default.
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• W2324729880 doi "https://doi.org/10.1038/sj.bjc.6600927" @default.
• W2324729880 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2377108" @default.
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