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• W2901161404 abstract "78 Pancreatic cancer is a devastating malignancy for which treatment and detection remain enigmatic. New diagnostic markers, therapeutics, and a better understanding of disease progression are urgently required to improve survival of patients. The mucin glycoproteins are a family of diverse molecules that have enabled us to detect cancers in relation to their normal tissue counterparts. One such mucin, mucin 17 (MUC17), is detected in pancreatic cancer tissues, which sharply contrasts the absence of MUC17 expression in the normal pancreas. We hypothesized that specific pathways, which are associated with expression of MUC17, control its aberrant expression and are activated in pancreatic cancer. To determine the significance of MUC17 expression in pancreatic cancer, it was necessary to define the underlying molecular mechanisms implicated in its aberrant expression. The pancreatic adenocarcinoma AsPC-1 cell line was used to investigate which signaling pathways contribute to MUC17 expression. Our data show that a 1,168 bp region proximal to the MUC17 coding sequence contains both promoter and enhancer activities. The MUC17 transcription initiator was identified and confirmed by primer extension analysis. Transcription initiates 54bp upstream of the ATG codon previously identified as the translation initiation site (Moniaux N., et al. 2006, 281, 23676-23685). Using databases, potential transcription factor binding sites (including those for: VDR/RXR heterodimers, NFκB, SMAD3, SMAD4, CDX-2, PDX-1, MZF-1, KLFs, GATA-1, AP-1, and growth factor responsiveness) were identified. Luciferase reporter assay results in AsPC-1 cells provide evidence that the cytokines, TNF-α and IL-6, and the growth factors, TGFβ-1, TGFβ-2, and EGF, are capable of activating transcription by increasing enhancer and/or basal promoter activities. Quantitative real-time PCR and western blotting demonstrate that an observed increase in MUC17 message results in increased production of MUC17 at the protein level, via activation by exogenous cytokines and growth factors and is dose and time dependent. Our results also provide evidence that combinations of growth factors (EGF + TGFβ-1) or growth factor and cytokine (TGFβ-2 + IL-6) up regulate MUC17 in an additive manner. Of particular interest is that when the cytokine TNF-α is combined with growth factors (+EGF, +TGFβ-1, or +TGFβ-2) a general decrease in MUC17 expression is observed (below that of TNF-α or growth factor treatment alone). This suggests that a counter mechanism exists for the down regulation of MUC17. MUC17 expression in the presence of growth factors or IL-6 may decrease if signals such as TNF-α are produced. Additional studies are underway to determine if expression of MUC17 is involved in the progression of disease or is lost as the result of developing inflammation associated with ductal pancreatic cancer (work, in part, was supported by the NIH grants UO1 CA 111294 and T32 CA09476)." @default.
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• W2901161404 date "2008-05-01" @default.
• W2901161404 modified "2023-09-26" @default.
• W2901161404 title "Regulation of human mucin MUC17 expression in pancreatic adenocarcinoma cells" @default.
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