论文部分内容阅读
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.The influence of nicotine on migration of gastric cancer cells was evaluated by trans-well assay and wound-healing migration assay.Receptor-mediated migration was studied by both inhibitor and small interfering RNA.Alpha7 nicotinic acetylcholine receptor, alpha7-nAChR, was identified in gastric cancer cell lines, AGS cells.Nicotine enhanced AGS cell migration in trans-well 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 down-regulation E-cadherin and up-regulation ZEB-1 and snail.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, the patients with gastric cancer should avoid from smoking.