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Vol 78, No 4 (2010)
ORIGINAL PAPERS
Published online: 2010-07-08
Submitted: 2013-02-22
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Cell phenotype determines PAI-1 antiproliferative effect - suppressed proliferation of the lung cancer but not prostate cancer cells

Joanna Chorostowska-Wynimko, Marta Kędzior, Radosław Struniawski, Paulina Jaguś, Ewa Skrzypczak-Jankun, Jerzy Jankun
Pneumonol Alergol Pol 2010;78(4):279-283.

open access

Vol 78, No 4 (2010)
ORIGINAL PAPERS
Published online: 2010-07-08
Submitted: 2013-02-22

Abstract


Introduction: Plasminogen inhibitor activator type 1 (PAI-1) is an important regulator of tumor growth and metastasis formation acting directly via specific urokinase complexing or indirectly due to its affinity to vitronectin. We have shown previously that PAI-1 modifies angiogenic activity of endothelial cells in a dose-dependent manner but also in close relationship to the cell phenotype. Present study aimed on evaluating the PAI-1 effect on the proliferative activity of lung cancer cells (A549), prostate cancer cells (DU145) as well as endothelial cells (HUVEC).
Results: Mutated PAI-1 (1, 10, 100 μg/mL) characterized by the prolonged antifibrinolytic activity (T1/2 ~ 7000 h) inhibited proliferation of lung cancer A549 cells in a dose-dependent (p < 0.001) and time-dependent (p < 0.001) manner. No significant effect on the DU145 prostate cancer cells has been observed except of the 72 h cultures with highest PAI-1 concentration (100 μg/ml) (p < 0.001). Proliferative activity of endothelial cells (HUVEC) was affected by 100 μg/ml PAI-1 only, and independent of the culture period (24, 48 and 72 h, p < 0.001).
Conclusion: Plasminogen inhibitor activator type 1 modulates cell proliferation via antifibrynolitic mechanizm time- and dose-dependently, however final outcome is strongly affected by the cell phenotype.
Pneumonol. Alergol. Pol. 2010; 78, 4: 279-283

Abstract


Introduction: Plasminogen inhibitor activator type 1 (PAI-1) is an important regulator of tumor growth and metastasis formation acting directly via specific urokinase complexing or indirectly due to its affinity to vitronectin. We have shown previously that PAI-1 modifies angiogenic activity of endothelial cells in a dose-dependent manner but also in close relationship to the cell phenotype. Present study aimed on evaluating the PAI-1 effect on the proliferative activity of lung cancer cells (A549), prostate cancer cells (DU145) as well as endothelial cells (HUVEC).
Results: Mutated PAI-1 (1, 10, 100 μg/mL) characterized by the prolonged antifibrinolytic activity (T1/2 ~ 7000 h) inhibited proliferation of lung cancer A549 cells in a dose-dependent (p < 0.001) and time-dependent (p < 0.001) manner. No significant effect on the DU145 prostate cancer cells has been observed except of the 72 h cultures with highest PAI-1 concentration (100 μg/ml) (p < 0.001). Proliferative activity of endothelial cells (HUVEC) was affected by 100 μg/ml PAI-1 only, and independent of the culture period (24, 48 and 72 h, p < 0.001).
Conclusion: Plasminogen inhibitor activator type 1 modulates cell proliferation via antifibrynolitic mechanizm time- and dose-dependently, however final outcome is strongly affected by the cell phenotype.
Pneumonol. Alergol. Pol. 2010; 78, 4: 279-283
Get Citation

Keywords

PAI-1; lung cancer; prostate cancer; HUVEC

About this article
Title

Cell phenotype determines PAI-1 antiproliferative effect - suppressed proliferation of the lung cancer but not prostate cancer cells

Journal

Advances in Respiratory Medicine

Issue

Vol 78, No 4 (2010)

Pages

279-283

Published online

2010-07-08

Bibliographic record

Pneumonol Alergol Pol 2010;78(4):279-283.

Keywords

PAI-1
lung cancer
prostate cancer
HUVEC

Authors

Joanna Chorostowska-Wynimko
Marta Kędzior
Radosław Struniawski
Paulina Jaguś
Ewa Skrzypczak-Jankun
Jerzy Jankun

References (20)
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