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Abstract: Poster Presentations |

THE PROLIFERATION OF NON-SMALL LUNG CANCER INDUCED 4-(N-METHYL-N-NITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE (NNK) CAN BE OFFSET BY TROGLITAZONE, A LIGAND OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA FREE TO VIEW

M. Y. Li, MSc; Johnson Yip, MSc; T. W. Lee, MBBS; A. P. Yim, MD; George G. Chen, MD, PhD*
Author and Funding Information

The Chinese University of Hong Kong, Shatin NT, Hong Kong PRC



Chest. 2006;130(4_MeetingAbstracts):234S. doi:10.1378/chest.130.4_MeetingAbstracts.234S-c
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Abstract

PURPOSE: Our previous study showed that peroxisome proliferator-activated receptor (PPAR) gamma induced the growth arrest and apoptosis of lung cancer cells. However, whether PPAR gamma ligands can inhibit the growth-promoting function of NNK is unknown.

METHODS: To address the above question, we used NCI-H23 lung cancer cells as the model to study how troglitazone (TGZ), a ligand of PPAR gamma, influenced the function of NNK.

RESULTS: Results showed that NNK stimulated cell proliferation, induced the DNA binding activity of nuclear factor-kB (NF-kB), down-regulated Bad expression, and up-regulated PPAR gamma protein expressions. Inhibition of NF-kB nuclear translocation led to the suppression of NNK-mediated Bad expression, indicating that NNK may regulate Bad expression through the activation of NF-kB. TGZ significantly inhibited cell proliferation induced by NNK. Though TGZ did not affect NF-kB activity, it up-regulated Bad expression.

CONCLUSION: Taken together, TGZ can efficiently inhibit the proliferation of lung cancer cells induced by NNK via Bad- and PPAR gamma-related pathways, which may not be directly relevant to the activity of NF-kB.

CLINICAL IMPLICATIONS: The finding may help to develop a new therapy for lung cancer.

DISCLOSURE: George Chen, None.

Wednesday, October 25, 2006

12:30 PM - 2:00 PM


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