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- W2312911855 abstract "Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, ILCancer cells, especially adenocarcinomas, express aberrant forms of mucins, as compared to their normal cell counterparts. These aberrant forms arise as a consequence of transformation-related alterations in expression of mucin mRNAs including alternative splice forms, and deregulation of enzymes that post-translationally modify mucin core proteins. Previous work has established that MUC1 is overexpressed and differentially glycosylated in adenocarcinomas and that this overexpression is associated with aggressive forms of pancreatic cancer. Most studies have focused on the full-length MUC1 isoform that contains the VNTR and all seven exons, but alternative splicing of MUC1 yields a minimum of 30 isoforms, of which several have been linked to malignancy in ovarian, cervical, and breast cancer. We evaluated expression of MUC1 alternate splice forms in a series of isogenic clonal pancreatic cancer cell lines that exhibit different properties of morphological differentiation, tumor growth and metastasis. The results revealed significant variation in splice variant expression between these isogenic cell lines and has implicated an association between isoform expression and metastatic potential. The knockdown of specific splice variants and MUC1 isoform families in S2-007 pancreatic cancer cells suggested that individual isoforms show differential capacity for regulating expression of target genes and miRNAs, which in turn led to differences in tumor growth rate and metastatic potential. Specifically, the stable knockdown of all members of the MUC1 X-family significantly altered expression of miRNAs 193b and 320 and reduced tumor growth in a pancreatic cancer animal model. MUC1 X-family also affected expression levels of several genes associated with Gemcitabine resistance and both pro and anti-inflammatory pathways that are predicted to influence disease progression and tumor associated immunosuppression.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1304. doi:1538-7445.AM2012-1304" @default.
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- W2312911855 date "2012-04-15" @default.
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- W2312911855 title "Abstract 1304: Specific MUC1 isoforms function to regulate gene expression and tumor growth in pancreatic cancer" @default.
- W2312911855 doi "https://doi.org/10.1158/1538-7445.am2012-1304" @default.
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