Published ahead of print on October 27, 2005, doi:10.1165/rcmb.2005-0117OC Am. J. Respir. Cell Mol. Biol., Volume 34, Number 3, March 2006, 264-273 A more recent version of this article appeared on March 1, 2006
Submitted on March 28, 2005 Cigarette Smoking Induces Overexpression of HGF in Type II Pneumocytes and Lung Cancer CellsJin-Tang Chen1,1 Department of Health, Feng-Yuan Hospital, Feng-Yuan, Taiwan, 2 Department of Surgery, Chang-Hua Christian Hospital, Chang-Hua, Taiwan, 3 Graduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan, 4 Graduate Institute of Veterinary Microbiology, National Chung Hsing University, Taichung, Taiwan, 5 Department of Health, Hsin Chu General Hospital, Hsin-Chu, Taiwan, 6 Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan * To whom correspondence should be addressed. E-mail: kcchow{at}dragon.nchu.edu.tw.
We examined gene expression of hepatocyte growth factor (HGF) and HGF receptor (HGFR, or product of c-met) in smokers and non-smokers with adenocarcinoma (ADC) by suppression subtractive hybridization (SSH) and microarray techniques. Expression of HGF and c-met was confirmed by reverse transcription-polymerase chain reaction (RT-PCR). HGF content in the respective tumor mass and non-tumor lung tissue was measured by enzyme-linked immunosorbent assay (ELISA). HGF in pathological samples was localized by immunohistochemistry and in situ hybridization (ISH). Our results indicated that overexpression of HGFR was frequently detected in ADC cells, while that of HGF was in alveolar type II (ATII) cells. Interestingly, overexpression of HGF was correlated with cigarette smoking and tumor stages. In vitro, HGF expression was evaluated in isolated murine ATII cells as well as 12 ADC cell lines, and we found that nicotine activated HGF expression in both ATII cells and lung cancer cells.
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