This Article Full Text Full Text (PDF) All Versions of this Article: 2005-0117OCv1 34/3/264    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, J.-T. Articles by Chen, C.-Y. Search for Related Content PubMed PubMed Citation Articles by Chen, J.-T. Articles by Chen, C.-Y.

Cigarette Smoking Induces Overexpression of Hepatocyte Growth Factor in Type II Pneumocytes and Lung Cancer Cells

Department of Health, Feng-Yuan Hospital, Feng-Yuan; Department of Surgery, Chang-Hua Christian Hospital, Chang-Hua; Graduate Institute of Biomedical Sciences and Graduate Institute of Veterinary Microbiology, National Chung Hsing University, and Department of Surgery, Taichung Veterans General Hospital; Department of Health Care Administration, Central Taiwan University of Science and Technology, Taichung; and Department of Health, Hsin Chu General Hospital, Hsin Chu, Taiwan

Correspondence and requests for reprints should be addressed to Kuan-Chih Chow, Graduate Institute of Biomedical Sciences, National Chung Hsing University, 250 Kuo-Kuang Road, Taichung, 40227 Taiwan. E-mail: kcchow{at}dragon.nchu.edu.tw

We examined gene expression of hepatocyte growth factor (HGF) and HGF receptor (HGFR), or product of proto-oncogene c-met (c-met), in smokers and nonsmokers with adenocarcinoma (ADC) by suppression subtractive hybridization and microarray techniques. Expression of HGF and c-met was confirmed by RT-PCR. HGF content in the respective tumor mass and nontumor lung tissue was measured by ELISA. HGF in pathologic samples was localized by immunohistochemistry and in situ hybridization. Our results indicate that overexpression of HGFR was frequently detected in ADC cells, whereas overexpression of HGF was detected in alveolar type II (ATII) cells. Overexpression of HGF was correlated with cigarette smoking and tumor stages. In vitro, HGF expression was evaluated in isolated murine ATII cells and in 12 ADC cell lines, and we found that nicotine activated HGF expression in ATII cells and lung cancer cells.

Key Words: immunohistochemistry • in situ hybridization • microarray • suppression subtractive hybridization • type II pneumocyte

This article has been cited by other articles:

				J.-T. Chen, C.-Y. Huang, Y.-Y. Chiang, W.-H. Chen, S.-H. Chiou, C.-Y. Chen, and K.-C. Chow HGF Increases Cisplatin Resistance via Down-Regulation of AIF in Lung Cancer Cells Am. J. Respir. Cell Mol. Biol., May 1, 2008; 38(5): 559 - 565. [Abstract] [Full Text] [PDF]

				K.-C. Chow Correspondence The Pulmonary Source of Hepatocyte Growth Factor in Non-Small Cell Lung Cancer Am. J. Respir. Cell Mol. Biol., January 1, 2007; 36(1): 131 - 132. [Full Text] [PDF]

				M. Bonay, A. Boutten, and B. Crestani HGF and Lung Carcinoma: Don't Forget Neutrophils. Am. J. Respir. Cell Mol. Biol., May 1, 2006; 34(5): 643 - 643. [Full Text] [PDF]