Effects of chemotherapeutic drugs and TRAIL (tumor necrosis factor-related apoptosis inducing ligand) on the non-small lung cancer cells

C. C. Tu, W. J. Wu (Taichung, Taiwan)

Source: Annual Congress 2009 - Treatment of lung cancer
Session: Treatment of lung cancer
Session type: Thematic Poster Session
Number: 2641
Disease area: Thoracic oncology

Congress or journal article abstract

Abstract

Intensive chemotherapy regimens do effectively kill lung cancer cerlls. However, lung cancer cells are often resistance to chemotherapy and even develop acquired chemoresistance or show multi-drug resistance as a consequence of the previous treatment. TRAIL is a new proapoptotic cytokine. It is believed that TRAIL can selectively kill cancer cells but not normal cells. The aim of our study was to determine the effect of combination therapy with chemotherapeutic agents and TRAIL in different lung cancer cells lines and in vivo.
The sensitivity of NSCLC undergo apoptosis was assessed by MTT assay, DAPI assay and PI staining.
Firstly, we test the sensitivity of different cancer cells lines to TRAIL. Our results show that H460 is most sensitive to TRAIL; H1299 is most resistance to TRAIL. In the syngergistic effects of chemotherapeutic agents and TRAIL-induced apoptosis in NSCLC cell lines, there is also significant synergistic effect. Paclitabine enhances cytotoxic effect of TRAIL in 7 of 10 cell lines. Gemcitabine and TRAIL are synergistic in 6 of 10 NSCLC cell lines. Cisplatin and TRAIL are synergistic in 3 of 10 NSCLC cell lines. Finally, in vivo administration of paclitaxel and TRAIL substantially inhibited subcutaneous tumor growth of H460 cells.
Our results suggest that TRAIL is a promising anti-tumor cytokine that has significant synergistic effects with conventional chemotherapeutic drugs against human NSCLC.


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Citations should be made in the following way:
C. C. Tu, W. J. Wu (Taichung, Taiwan). Effects of chemotherapeutic drugs and TRAIL (tumor necrosis factor-related apoptosis inducing ligand) on the non-small lung cancer cells. Eur Respir J 2009; 34: Suppl. 53, 2641

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