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Published ahead of print on December 20, 2007, doi:10.1165/rcmb.2007-0001OC

Am. J. Respir. Cell Mol. Biol., Volume 38, Number 5, May 2008, 559-565

A more recent version of this article appeared on May 1, 2008
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Submitted on January 2, 2007
Revised on December 12, 2007

HGF Increases Cisplatin Resistance via Down-Regulation of AIF in Lung Cancer Cells

Jin-Tang Chen1, Chih-Yang Huang2, Yung-Yen Chiang3, Wen-Heng Chen4, Shiow-Her Chiou2, Chih-Yi Chen5, and Kuan-Chih Chow6*

1 Feng-Yuan Hospital, Feng-Yuan, Taiwan, 2 Graduate Institute of Veterinary Microbiology, National Chung Hsing University, Taichung, Taiwan, 3 Department of Dental Laboratory Technology, Central Taiwan University of Science and Technology, Taichung, Taiwan, 4 Graduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan, 5 Comprehensive Cancer Center, China Medical University Hospital, Taichung, Taiwan, 6 Comprehensive Cancer Center, China Medical University Hospital, Taichung, Taiwan; Graduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan

* To whom correspondence should be addressed. E-mail: kcchow{at}dragon.nchu.edu.tw.

Our previous study had shown that advanced stages of lung adenocarcinomas (ADC) was frequently associated with overexpression of hepatocyte growth factor (HGF), which has multipotent and anti-apoptotic activities. In this study, we examined the effect of HGF on gene expression of apoptosis-inducing factor (AIF) and cisplatin sensitivity in lung ADC cells. Expression of AIF was determined by immunocytochemistry and confocal immunofluorescence microscopy. Our data show that addition of HGF suppressed AIF expression and increased cisplatin resistance. The effect could be through HGF receptor and its down-stream effector, focal adhesion kinase (FAK). Interestingly, knockout of FAK gene increased AIF expression and drug sensitivity. Re-introduction of FAK gene, on the other hand, restored drug resistance. These results suggested that HGF might induce cisplatin resistance via c-Met to activate FAK and down-regulate AIF expression.






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Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2007 American Thoracic Society.