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General Physiology and Biophysics 2009 General Physiology and Biophysics Vol.28, No.3, p.294–301, 2009
General Physiology and Biophysics 2009 General Physiology and Biophysics Vol.28, No.3, p.294–301, 2009
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General Physiology and Biophysics Vol.28, No.3, p.294–301, 2009 |
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| Title: Modulation of cell proliferation and differentiation of human lung carcinoma cells by the interferon-alpha | ||
| Author: Daniela Krejčová, Jiřina Procházková, Lukáš Kubala and Jiří Pacherník | ||
| Abstract: Treatments of non-small cell lung cancer (NSCLC), the most common form of lung cancer, still remain poor. Interferon alpha (IFN-α), an important physiological immunomodulator, possesses direct cytotoxic and cytostatic effects on tumour cells, antiangiogenic effects, and activates anti-tumour immunity. Recently, the IFN-α oncologic indications have included melanoma, renal carcinoma, and different types of leukaemia. However, the application of IFN-α in therapy of lung cancer has not been validated yet. Herein the human lung carcinoma cell line A549, a model of NSCLC in vitro, was used to pursue the effect of IFN-α on A549 cell proliferation and differentiation together with the effect on protein expression and activity of three ATP-transporters mediating multi-drug resistance (MDR). IFN-α significantly inhibited the proliferation of A549 cells which was not connected with arrest in a particular cell cycle phase. Further, IFN-α-mediated differentiation of A549 was observed based on an increase in alkaline phosphatase activity. Simultaneously, IFN-α increased the expression and activity of ATP-transporters mediating MDR. Thus, the IFN-α down-regulation of NSCLC cell proliferation was accompanied by a potential of cells to exclude potential therapeutic substances such as chemotherapeutic agents. These effects could have a significant impact on considerations of IFN-α as a therapeutic agent for NSCLC. |
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| Keywords: Non-small cell lung cancer — ABC transporter proteins — Cell cycle — Interferons | ||
| Year: 2009, Volume: 28, Issue: 3 | Page From: 294, Page To: 301 | |
| doi:10.4149/gpb_2009_03_294 |
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