Abstract

Background/purpose: The tobacco-specific mitogen nicotine was reported to correlate with cancer progression and tumorigenesis in breast cancer. Metastasis is a major cause of cancer death, so the influence of nicotine on breast cancer cell migration is also of interest. Our aim is to elucidate the mechanisms of nicotine-enhanced migration of breast cancer cells and thereby achieve better control of metastasis. Methods: The influence of nicotine on breast cancer cell migration was evaluated by trans-well and wound-healing migration assays. Receptor-mediated migration was studied with both a small molecule inhibitor and small interfering RNA (siRNA). Results: The alpha9 nicotinic acetylcholine receptor, α9nAChR, was identified in breast cancer cell lines MCF-7 and MDA-MB-231. Nicotine enhanced cell migration in both trans-well and wound-healing migration assays. We used a specific inhibitor and siRNA to demonstrate that α9nAChR is the key modulator in mediating nicotine-enhanced breast cancer cell migration through up-regulation of fibronectin and vimentin. Conclusion: Nicotine treatment enhanced breast cancer metastasis through α9nAChR signaling via enhanced fibronectin and vimentin expression.

Original languageEnglish
Pages (from-to)283-292
Number of pages10
JournalJournal of Experimental and Clinical Medicine(Taiwan)
Volume3
Issue number6
DOIs
Publication statusPublished - Dec 2011

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Nicotinic Receptors
Nicotine
Breast Neoplasms
Neoplasm Metastasis
Cell Movement
Neoplasms
Vimentin
Fibronectins
Wound Healing
Small Interfering RNA
Mitogens
Tobacco
Cause of Death
Carcinogenesis
Up-Regulation
Cell Line

Keywords

  • Breast cancer
  • Epithelial-to-mesenchymal transition (EMT)
  • Migration
  • Nicotine
  • Nicotinic acetylcholine receptor (nAChR)
  • Smoking

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{d22f851897d64ae79e0ff1d04c37c96c,
title = "The alpha9 nicotinic acetylcholine receptor is the key mediator in nicotine-enhanced cancer metastasis in breast cancer cells",
abstract = "Background/purpose: The tobacco-specific mitogen nicotine was reported to correlate with cancer progression and tumorigenesis in breast cancer. Metastasis is a major cause of cancer death, so the influence of nicotine on breast cancer cell migration is also of interest. Our aim is to elucidate the mechanisms of nicotine-enhanced migration of breast cancer cells and thereby achieve better control of metastasis. Methods: The influence of nicotine on breast cancer cell migration was evaluated by trans-well and wound-healing migration assays. Receptor-mediated migration was studied with both a small molecule inhibitor and small interfering RNA (siRNA). Results: The alpha9 nicotinic acetylcholine receptor, α9nAChR, was identified in breast cancer cell lines MCF-7 and MDA-MB-231. Nicotine enhanced cell migration in both trans-well and wound-healing migration assays. We used a specific inhibitor and siRNA to demonstrate that α9nAChR is the key modulator in mediating nicotine-enhanced breast cancer cell migration through up-regulation of fibronectin and vimentin. Conclusion: Nicotine treatment enhanced breast cancer metastasis through α9nAChR signaling via enhanced fibronectin and vimentin expression.",
keywords = "Breast cancer, Epithelial-to-mesenchymal transition (EMT), Migration, Nicotine, Nicotinic acetylcholine receptor (nAChR), Smoking",
author = "Chin-Sheng Hung and Peng, {Yu Jin} and Po-Li Wei and Chia-Hwa Lee and Su, {Hou Yu} and Yuan-Soon Ho and Shyr-Yi Lin and Chih-Hsiung Wu and Yu-Jia Chang",
year = "2011",
month = "12",
doi = "10.1016/j.jecm.2011.10.008",
language = "English",
volume = "3",
pages = "283--292",
journal = "Journal of Experimental and Clinical Medicine",
issn = "1878-3317",
publisher = "Elsevier Taiwan LLC",
number = "6",

}

TY - JOUR

T1 - The alpha9 nicotinic acetylcholine receptor is the key mediator in nicotine-enhanced cancer metastasis in breast cancer cells

AU - Hung, Chin-Sheng

AU - Peng, Yu Jin

AU - Wei, Po-Li

AU - Lee, Chia-Hwa

AU - Su, Hou Yu

AU - Ho, Yuan-Soon

AU - Lin, Shyr-Yi

AU - Wu, Chih-Hsiung

AU - Chang, Yu-Jia

PY - 2011/12

Y1 - 2011/12

N2 - Background/purpose: The tobacco-specific mitogen nicotine was reported to correlate with cancer progression and tumorigenesis in breast cancer. Metastasis is a major cause of cancer death, so the influence of nicotine on breast cancer cell migration is also of interest. Our aim is to elucidate the mechanisms of nicotine-enhanced migration of breast cancer cells and thereby achieve better control of metastasis. Methods: The influence of nicotine on breast cancer cell migration was evaluated by trans-well and wound-healing migration assays. Receptor-mediated migration was studied with both a small molecule inhibitor and small interfering RNA (siRNA). Results: The alpha9 nicotinic acetylcholine receptor, α9nAChR, was identified in breast cancer cell lines MCF-7 and MDA-MB-231. Nicotine enhanced cell migration in both trans-well and wound-healing migration assays. We used a specific inhibitor and siRNA to demonstrate that α9nAChR is the key modulator in mediating nicotine-enhanced breast cancer cell migration through up-regulation of fibronectin and vimentin. Conclusion: Nicotine treatment enhanced breast cancer metastasis through α9nAChR signaling via enhanced fibronectin and vimentin expression.

AB - Background/purpose: The tobacco-specific mitogen nicotine was reported to correlate with cancer progression and tumorigenesis in breast cancer. Metastasis is a major cause of cancer death, so the influence of nicotine on breast cancer cell migration is also of interest. Our aim is to elucidate the mechanisms of nicotine-enhanced migration of breast cancer cells and thereby achieve better control of metastasis. Methods: The influence of nicotine on breast cancer cell migration was evaluated by trans-well and wound-healing migration assays. Receptor-mediated migration was studied with both a small molecule inhibitor and small interfering RNA (siRNA). Results: The alpha9 nicotinic acetylcholine receptor, α9nAChR, was identified in breast cancer cell lines MCF-7 and MDA-MB-231. Nicotine enhanced cell migration in both trans-well and wound-healing migration assays. We used a specific inhibitor and siRNA to demonstrate that α9nAChR is the key modulator in mediating nicotine-enhanced breast cancer cell migration through up-regulation of fibronectin and vimentin. Conclusion: Nicotine treatment enhanced breast cancer metastasis through α9nAChR signaling via enhanced fibronectin and vimentin expression.

KW - Breast cancer

KW - Epithelial-to-mesenchymal transition (EMT)

KW - Migration

KW - Nicotine

KW - Nicotinic acetylcholine receptor (nAChR)

KW - Smoking

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