Abstract
CD133 has been implicated as a cancer stem cell (CSC) surface marker in several malignancies including pancreatic cancer. However, the functional role of this surface glycoprotein in the cancer stem cell remains elusive. In this study, we determined that CD133 overexpression induced "stemness" properties in MIA-PaCa2 cells along with increased tumorigenicity, tumor progression, and metastasis in vivo. Additionally, CD133 expression induced epithelial-mesenchymal transition (EMT) and increased in vitro invasion. EMT induction and increased invasiveness were mediated by NF-κB activation, as inhibition of NF-κB mitigated these effects. This study showed that CD133 expression contributes to pancreatic cancer "stemness," tumorigenicity, EMT induction, invasion, and metastasis.
Highlights
Pancreatic cancer remains the only cancer type with a single-digit 5-year survival rate, a mere 6% [1]
Multiple studies done on colon cancer, liver cancer, gastric cancer, and neuroblastoma indicate that CD133 expression correlates to poor prognosis [2, 5, 6, 10,11,12], similar to what our studies showed in the KPC model
CD133 has been described as a surface marker of cancer stem cells in several cancer types [5, 21, 22]
Summary
Pancreatic cancer remains the only cancer type with a single-digit 5-year survival rate, a mere 6% [1]. Pancreatic cancer stem cells have been isolated and studied in multiple murine models since 2007 based on the expression of several markers present on the cell surface [2,3,4,5]. These included CD44, CD24, ESA, CD133, and c-Met, among others. Many studies have demonstrated that expression of CD133 correlates with poor patient prognosis in pancreatic cancer, as well as other cancer types [2, 5, 6]. High CD133 expression in these tumors seemed to be associated with poor prognosis of the cancer along with increased invasiveness [7]
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