Abstract

Background: Long-term cigarette smoking increases the risk of colorectal cancer mortality. Tobacco's addictive toxin, nicotine, was reported to increase DNA synthesis of colon cancer cells. Because metastasis is the major cause of cancer death, the influence of nicotine on the migration of colon cancer cells remains to be determined. Methods: The influence of nicotine on the migration of colon cancer cells was evaluated using transwell assay. Nicotine receptor-mediated migration was studied by using both inhibitors and small interfering RNA (siRNA). The role of COX-2 signal was studied using pharmacological inhibitors. The expression of epithelial mesenchymal transition (EMT) marker and COX-2 signal was evaluated using real-time polymerase chain reaction (PCR). Results: Nicotine enhanced DLD-1 and SW480 cell migration in a dose-dependent manner. We used inhibitors and siRNA to demonstrate that α7-nAChR mediates nicotine-enhanced colon cancer cell migration and upregulates fibronectin expression, which is involved in nicotine-enhanced migration. Furthermore, COX-2 signal was induced by nicotine treatment and is involved in nicotine-enhanced fibronectin expression. Conclusions: Nicotine, tobacco's additive toxin, enhances colon cancer metastasis through α7-nAChR and fibronectin-a mesenchymal marker for epithelial mesenchymal transition. Furthermore, COX-2 signal was involved in the induction of fibronectin. Therefore, smoking may play role in the progression of colon cancer.

Original languageEnglish
Pages (from-to)1782-1790
Number of pages9
JournalAnnals of Surgical Oncology
Volume18
Issue number6
DOIs
Publication statusPublished - Jun 2011

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Nicotine
Fibronectins
Colonic Neoplasms
Cell Movement
Epithelial-Mesenchymal Transition
Small Interfering RNA
Tobacco
Smoking
Neoplasm Metastasis
Real-Time Polymerase Chain Reaction
Cause of Death
Colorectal Neoplasms
Up-Regulation
Pharmacology
Mortality
DNA

ASJC Scopus subject areas

  • Surgery
  • Oncology

Cite this

Nicotine enhances colon cancer cell migration by induction of fibronectin. / Wei, Po Li; Kuo, Li Jen; Huang, Ming Te; Ting, Wen Chien; Ho, Yuan Soon; Wang, Weu; An, Jane; Chang, Yu Jia.

In: Annals of Surgical Oncology, Vol. 18, No. 6, 06.2011, p. 1782-1790.

Research output: Contribution to journalArticle

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abstract = "Background: Long-term cigarette smoking increases the risk of colorectal cancer mortality. Tobacco's addictive toxin, nicotine, was reported to increase DNA synthesis of colon cancer cells. Because metastasis is the major cause of cancer death, the influence of nicotine on the migration of colon cancer cells remains to be determined. Methods: The influence of nicotine on the migration of colon cancer cells was evaluated using transwell assay. Nicotine receptor-mediated migration was studied by using both inhibitors and small interfering RNA (siRNA). The role of COX-2 signal was studied using pharmacological inhibitors. The expression of epithelial mesenchymal transition (EMT) marker and COX-2 signal was evaluated using real-time polymerase chain reaction (PCR). Results: Nicotine enhanced DLD-1 and SW480 cell migration in a dose-dependent manner. We used inhibitors and siRNA to demonstrate that α7-nAChR mediates nicotine-enhanced colon cancer cell migration and upregulates fibronectin expression, which is involved in nicotine-enhanced migration. Furthermore, COX-2 signal was induced by nicotine treatment and is involved in nicotine-enhanced fibronectin expression. Conclusions: Nicotine, tobacco's additive toxin, enhances colon cancer metastasis through α7-nAChR and fibronectin-a mesenchymal marker for epithelial mesenchymal transition. Furthermore, COX-2 signal was involved in the induction of fibronectin. Therefore, smoking may play role in the progression of colon cancer.",
author = "Wei, {Po Li} and Kuo, {Li Jen} and Huang, {Ming Te} and Ting, {Wen Chien} and Ho, {Yuan Soon} and Weu Wang and Jane An and Chang, {Yu Jia}",
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T1 - Nicotine enhances colon cancer cell migration by induction of fibronectin

AU - Wei, Po Li

AU - Kuo, Li Jen

AU - Huang, Ming Te

AU - Ting, Wen Chien

AU - Ho, Yuan Soon

AU - Wang, Weu

AU - An, Jane

AU - Chang, Yu Jia

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N2 - Background: Long-term cigarette smoking increases the risk of colorectal cancer mortality. Tobacco's addictive toxin, nicotine, was reported to increase DNA synthesis of colon cancer cells. Because metastasis is the major cause of cancer death, the influence of nicotine on the migration of colon cancer cells remains to be determined. Methods: The influence of nicotine on the migration of colon cancer cells was evaluated using transwell assay. Nicotine receptor-mediated migration was studied by using both inhibitors and small interfering RNA (siRNA). The role of COX-2 signal was studied using pharmacological inhibitors. The expression of epithelial mesenchymal transition (EMT) marker and COX-2 signal was evaluated using real-time polymerase chain reaction (PCR). Results: Nicotine enhanced DLD-1 and SW480 cell migration in a dose-dependent manner. We used inhibitors and siRNA to demonstrate that α7-nAChR mediates nicotine-enhanced colon cancer cell migration and upregulates fibronectin expression, which is involved in nicotine-enhanced migration. Furthermore, COX-2 signal was induced by nicotine treatment and is involved in nicotine-enhanced fibronectin expression. Conclusions: Nicotine, tobacco's additive toxin, enhances colon cancer metastasis through α7-nAChR and fibronectin-a mesenchymal marker for epithelial mesenchymal transition. Furthermore, COX-2 signal was involved in the induction of fibronectin. Therefore, smoking may play role in the progression of colon cancer.

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