Abstract 2454: Pancreatic cancer stem cells (CSCs) express MUC1 and MUC1-expressing pancreatic cancers encompass higher levels of CSCs

Abstract

Abstract Introduction: Pancreatic ductal adenocarcinoma (PDA) has the worst prognosis of all cancers and is the fourth leading cause of cancer-related deaths in the United States. Cancer stem cells (CSCs), which are a small population of tumor cells that have the ability to self-renew and differentiate into the diverse cells that comprise the tumor, have been identified in pancreatic cancer patients as lineage-negative, CD133 (prominin-1)-expressing cells. In pancreatic cancer, MUC1 is a protein expressed with a high frequency and its expression correlates with high metastasis and poor prognosis. Recent reports from our lab have demonstrated the ability of MUC1 to drive epithelial-to-mesenchymal transition thus producing a cell with ‘stem-like’ properties. We therefore investigated the correlation between MUC1 expression and CSCs. Methods: Primary tumor tissues surgically resected from patients diagnosed with pancreatic adenocarcinoma (n=8) and human pancreatic cancer cell lines were assessed for CD133 and MUC1 expression by flow cytometry. Results: In pancreatic cancer patients, tumor MUC1 levels correlated with a higher percentage of CD133-expressing cells (R=0.76). Similarly, in MiaPaCa2, Capan-1, BxPC3 WT, BxPC3 MUC1, Su86.86 WT and Su86.86 MUC1 cells lines, MUC1 levels correlated with increased CD133 expression (R=0.83). The majority of CD133+ cells isolated from primary human pancreatic tumors (82.6 ± 12.7%) expressed MUC1. Similar results were obtained using cell lines, as 83.22 ± 30.9% of CD133-expressing cells were MUC1-positive. Conclusion: MUC1 is present on the majority of CSCs and its expression correlates with higher levels of cancer stem cells. This study demonstrates yet another oncogenic role of MUC1 in pancreatic cancer progression and suggests MUC1 as a novel marker for CSCs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2454. doi:10.1158/1538-7445.AM2011-2454