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 languageEnglish
Pages (from-to)2671-2679
Number of pages9
JournalAnnals of Surgical Oncology
Volume18
Issue number9
DOIs
Publication statusPublished - Sep 2011

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alpha7 Nicotinic Acetylcholine Receptor
Nicotine
Stomach Neoplasms
Cell Movement
Cadherins
Mitogens
Wound Healing
Small Interfering RNA
Tobacco
Smoking
Neoplasm Metastasis
Epithelial-Mesenchymal Transition
Snails
Cause of Death
Neoplasms
Up-Regulation
Down-Regulation

ASJC Scopus subject areas

  • Surgery
  • Oncology

Cite this

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 journalArticle

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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.",
author = "Lien, {Yung Chang} and Weu Wang and Kuo, {Li Jen} and Liu, {Jun Jen} and Wei, {Po Li} and Ho, {Yuan Soon} and Ting, {Wen Chien} and Wu, {Chih Hsiung} and Chang, {Yu Jia}",
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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

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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.

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