Erschienen in:
01.09.2011 | Translational Research and Biomarkers
Nicotine Promotes Cell Migration Through Alpha7 Nicotinic Acetylcholine Receptor in Gastric Cancer Cells
verfasst von:
Yung-Chang Lien, MD, Weu Wang, MD, Li-Jen Kuo, MD, Jun-Jen Liu, PhD, Po-Li Wei, MD, PhD, Yuan-Soon Ho, PhD, Wen-Chien Ting, MD, Chih-Hsiung Wu, MD, PhD, Yu-Jia Chang, PhD
Erschienen in:
Annals of Surgical Oncology
|
Ausgabe 9/2011
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Abstract
Background
The objective was to study the mechanism of nicotine-enhanced migration of gastric cancer cells. Long-term cigarette smoking increases the risk of gastric cancer mortality. Tobacco-specific mitogen, nicotine, was reported to correlate with cancer progression on gastric cancer. Since metastasis is the major cause of cancer death, the influence of nicotine on the migration of gastric cancer cells remains to be determined.
Materials and Methods
The influence of nicotine on migration of gastric cancer cells was evaluated by transwell assay and wound-healing migration assay. Receptor-mediated migration was studied by both inhibitor and small interfering RNA.
Results
Alpha7 nicotinic acetylcholine receptor, alpha7-nAChR, was identified in gastric cancer cell lines, AGS cells. Nicotine enhanced AGS cell migration in transwell assay and wound-healing migration assay in a dose-dependent manner. We used inhibitor and siRNA to demonstrate that alpha7-nAChR mediated nicotine-enhanced gastric cancer cell migration through downregulation E-cadherin and upregulation ZEB-1 and snail.
Conclusions
Tobacco-specific mitogen, nicotine, enhanced gastric cancer metastasis through alpha7-nAChR and suppression of E-cadherin level—one of the hallmarks of epithelial to mesenchymal transition. Therefore, patients with gastric cancer should avoid smoking.