Research Papers:

CD133 initiates tumors, induces epithelial-mesenchymal transition and increases metastasis in pancreatic cancer

Alice Nomura _, Sulagna Banerjee, Rohit Chugh, Vikas Dudeja, Masato Yamamoto, Selwyn M. Vickers and Ashok K. Saluja

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Oncotarget. 2015; 6:8313-8322. https://doi.org/10.18632/oncotarget.3228

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Alice Nomura1, Sulagna Banerjee1, Rohit Chugh1, Vikas Dudeja1, Masato Yamamoto1, Selwyn M. Vickers1, Ashok K. Saluja1

1Division of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, MN, USA

Correspondence to:

Ashok K. Saluja, e-mail: [email protected]

Keywords: CD133, pancreatic cancer, invasion, metastasis, NF-kB

Received: October 28, 2014     Accepted: January 27, 2015     Published: March 16, 2015


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.

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