Long-term cigarette smoking increases the risk of gastric cancer mortality. Nicotine and NNK, tobacco-specific mitogens, were 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. In addition, how to improve the therapeutic efficacy is the important issue for gastric cancer. Our preliminary results indicated that nicotine or NNK treatment can enhance the migratory ability on gastric cancer. The enhancement effect was mediated through nicotinic acetylcholine receptor (nAChR). Silence of alpha7-nAChR expression may inhibit the enhanced effect by nicotine or NNK treatment, indicating that nAChR may be the target for preventing gastric cancer migration. Further, we also found that down-regulation of nAChR increased the sensitivity to chemo-therapy. Those result suggested that nAChR may be the novel therapeutic target for gastric cancer therapy. In this grant, we plan to find out whether the expression levels of nAChR may be correlated with a) the malignancy of gastric cancer, b) the therapeutic response of gastric (chemo- and radiation-therapy), or c) the numbers of side population of cancer cells. We believe that this study may provide a new viewpoint for gastric cancer therapy and will give more information for clinical cancer therapy.
|Effective start/end date||8/1/13 → 7/31/14|