Open Access

Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model

  • Authors:
    • Konstantinos Kamposioras
    • Chrysiida Tsimplouli
    • Caroline Verbeke
    • Alan Anthoney
    • Argyro Daoukopoulou
    • Christos N. Papandreou
    • Nikolaos Sakellaridis
    • George Vassilopoulos
    • Spyros P. Potamianos
    • Vasiliki Liakouli
    • Gemma Migneco
    • Francesco Del Galdo
    • Konstantinos Dimas
  • View Affiliations

  • Published online on: November 21, 2018     https://doi.org/10.3892/ijo.2018.4640
  • Pages: 537-549
  • Copyright: © Kamposioras et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Caveolin‑1 (Cav‑1) expression has been shown to be associated with tumor growth and resistance to chemotherapy in pancreatic cancer. The primary aim of this study was to explore the significance of Cav‑1 expression in pancreatic cancer cells as compared to fibroblasts in relation to cancer cell proliferation and chemoresistance, both in vitro and in vivo, in an immunodeficient mouse model. We also aimed to evaluate the immunohistochemical expression of Cav‑1 in the epithelial and stromal component of pancreatic cancer tissue specimens. The immunohistochemical staining of poorly differentiated tissue sections revealed a strong and weak Cav‑1 expression in the epithelial tumor cells and stromal fibroblasts, respectively. Conversely, the well‑differentiated areas were characterized by a weak epithelial Cav‑1 expression. Cav‑1 downregulation in cancer cells resulted in an increased proliferation in vitro; however, it had no effect on chemoresistance and growth gain in vivo. By contrast, the decreased expression of Cav‑1 in fibroblasts resulted in a growth advantage and the chemoresistance of cancer cells when they were co‑injected into immunodeficient mice to develop mixed fibroblast/cancer cell xenografts. On the whole, the findings of this study suggest that the downregulation of Cav‑1 in fibroblasts is associated with an increased tumor proliferation rate in vivo and chemoresistance. Further studies are warranted to explore whether the targeting of Cav‑1 in the stroma may represent a novel therapeutic approach in pancreatic cancer.
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February-2019
Volume 54 Issue 2

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Kamposioras K, Tsimplouli C, Verbeke C, Anthoney A, Daoukopoulou A, Papandreou CN, Sakellaridis N, Vassilopoulos G, Potamianos SP, Liakouli V, Liakouli V, et al: Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model. Int J Oncol 54: 537-549, 2019
APA
Kamposioras, K., Tsimplouli, C., Verbeke, C., Anthoney, A., Daoukopoulou, A., Papandreou, C.N. ... Dimas, K. (2019). Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model. International Journal of Oncology, 54, 537-549. https://doi.org/10.3892/ijo.2018.4640
MLA
Kamposioras, K., Tsimplouli, C., Verbeke, C., Anthoney, A., Daoukopoulou, A., Papandreou, C. N., Sakellaridis, N., Vassilopoulos, G., Potamianos, S. P., Liakouli, V., Migneco, G., Del Galdo, F., Dimas, K."Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model". International Journal of Oncology 54.2 (2019): 537-549.
Chicago
Kamposioras, K., Tsimplouli, C., Verbeke, C., Anthoney, A., Daoukopoulou, A., Papandreou, C. N., Sakellaridis, N., Vassilopoulos, G., Potamianos, S. P., Liakouli, V., Migneco, G., Del Galdo, F., Dimas, K."Silencing of caveolin-1 in fibroblasts as opposed to epithelial tumor cells results in increased tumor growth rate and chemoresistance in a human pancreatic cancer model". International Journal of Oncology 54, no. 2 (2019): 537-549. https://doi.org/10.3892/ijo.2018.4640