Open Access

Effect of MUC1/β-catenin interaction on the tumorigenic capacity of pancreatic CD133+ cells

  • Authors:
    • Andreia Mota Sousa
    • Margarida Rei
    • Rita Freitas
    • Sara Ricardo
    • Thomas Caffrey
    • Leonor David
    • Raquel Almeida
    • Michael Anthony Hollingsworth
    • Filipe Santos‑Silva
  • View Affiliations

  • Published online on: July 20, 2016     https://doi.org/10.3892/ol.2016.4888
  • Pages: 1811-1817
  • Copyright: © Sousa et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Despite the fact that the biological function of cluster of differentiation (CD)133 remains unclear, this glycoprotein is currently used in the identification and isolation of tumor-initiating cells from certain malignant tumors, including pancreatic cancer. In the present study, the involvement of mucin 1 (MUC1) in the signaling pathways of a highly tumorigenic CD133+ cellular subpopulation sorted from the pancreatic cancer cell line HPAF‑II was evaluated. The expression of MUC1‑cytoplasmic domain (MUC1‑CD) and oncogenic signaling transducers (epidermal growth factor receptor, protein kinase C delta, glycogen synthase kinase 3 beta and growth factor receptor‑bound protein 2), as well as the association between MUC1 and β‑catenin, were characterized in HPAF‑II CD133+ and CD133low cell subpopulations and in tumor xenografts generated from these cells. Compared with HPAF CD133low cells, HPAF‑II CD133+ cancer cells exhibited increased tumorigenic potential in immunocompromised mice, which was associated with overexpression of MUC1 and with the accordingly altered expression profile of MUC1‑associated signaling partners. Additionally, MUC1‑CD/β-catenin interactions were increased both in the HPAF‑II CD133+ cell subpopulation and derived tumor xenografts compared with HPAF CD133low cells. These results suggest that, in comparison with HPAF CD133low cells, CD133+ cells exhibit higher expression of MUC1, which contributes to their tumorigenic phenotype through increased interaction between MUC1‑CD and β-catenin, which in turn modulates oncogenic signaling cascades.
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September-2016
Volume 12 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Sousa AM, Rei M, Freitas R, Ricardo S, Caffrey T, David L, Almeida R, Hollingsworth MA and Santos‑Silva F: Effect of MUC1/β-catenin interaction on the tumorigenic capacity of pancreatic CD133+ cells. Oncol Lett 12: 1811-1817, 2016.
APA
Sousa, A.M., Rei, M., Freitas, R., Ricardo, S., Caffrey, T., David, L. ... Santos‑Silva, F. (2016). Effect of MUC1/β-catenin interaction on the tumorigenic capacity of pancreatic CD133+ cells. Oncology Letters, 12, 1811-1817. https://doi.org/10.3892/ol.2016.4888
MLA
Sousa, A. M., Rei, M., Freitas, R., Ricardo, S., Caffrey, T., David, L., Almeida, R., Hollingsworth, M. A., Santos‑Silva, F."Effect of MUC1/β-catenin interaction on the tumorigenic capacity of pancreatic CD133+ cells". Oncology Letters 12.3 (2016): 1811-1817.
Chicago
Sousa, A. M., Rei, M., Freitas, R., Ricardo, S., Caffrey, T., David, L., Almeida, R., Hollingsworth, M. A., Santos‑Silva, F."Effect of MUC1/β-catenin interaction on the tumorigenic capacity of pancreatic CD133+ cells". Oncology Letters 12, no. 3 (2016): 1811-1817. https://doi.org/10.3892/ol.2016.4888