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.
| Original language | English |
|---|---|
| Pages (from-to) | 2671-2679 |
| Number of pages | 9 |
| Journal | Annals of Surgical Oncology |
| Volume | 18 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - Sep 2011 |
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ASJC Scopus subject areas
- Surgery
- Oncology
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Nicotine promotes cell migration through alpha7 nicotinic acetylcholine receptor in gastric cancer cells. / Lien, Yung Chang; Wang, Weu; Kuo, Li Jen; Liu, Jun Jen; Wei, Po Li; Ho, Yuan Soon; Ting, Wen Chien; Wu, Chih Hsiung; Chang, Yu Jia.
In: Annals of Surgical Oncology, Vol. 18, No. 9, 09.2011, p. 2671-2679.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nicotine promotes cell migration through alpha7 nicotinic acetylcholine receptor in gastric cancer cells
AU - Lien, Yung Chang
AU - Wang, Weu
AU - Kuo, Li Jen
AU - Liu, Jun Jen
AU - Wei, Po Li
AU - Ho, Yuan Soon
AU - Ting, Wen Chien
AU - Wu, Chih Hsiung
AU - Chang, Yu Jia
PY - 2011/9
Y1 - 2011/9
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=80052747360&partnerID=8YFLogxK
U2 - 10.1245/s10434-011-1598-2
DO - 10.1245/s10434-011-1598-2
M3 - Article
C2 - 21347787
AN - SCOPUS:80052747360
VL - 18
SP - 2671
EP - 2679
JO - Annals of Surgical Oncology
JF - Annals of Surgical Oncology
SN - 1068-9265
IS - 9
ER -