Tea polyphenol (-)-epigallocatechin-3-gallate inhibits nicotine- and estrogen-induced α9-nicotinic acetylcholine receptor upregulation in human breast cancer cells

Shih Hsin Tu, Chung Yu Ku, Chi Tang Ho, Ching Shyang Chen, Ching Shui Huang, Chia Hwa Lee, Li Ching Chen, Min Hsiung Pan, Hui Wen Chang, Chien Hsi Chang, Yu Jia Chang, Po Li Wei, Chih Hsiung Wu, Yuan Soon Ho

Research output: Contribution to journalArticle

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Abstract

Scope: The aim of this research was to explore whether the tea-polyphenol (-)-epigallocatechin-3-gallate (EGCG) could be used as a potential agent for blocking smoking (nicotine, Nic)- or hormone (estradiol, E2)-induced breast cancer cell proliferation through inhibition of a common signaling pathway. Methods and results: To explore whether Nic (>0.1 μM, 24 h) and E2 (>1 nM, 24 h) significantly increased α9-nicotinic acetylcholine (α9-nicotinic acetylcholine receptor (nAChR)) mRNA and protein expression levels, real-time PCR and immunoblotting analysis experiments were performed in human breast cancer (MCF-7) cells. Luciferase promoter activity experiment was performed to test the α9-nAChR promoter activity affected by Nic, E2 or EGCG. The results indicate that treatment with EGCG (1 μM) profoundly decreases Nic- and E2-induced MCF-7 proliferation by down regulating α9-nAChR expression. The α9-nAChR promoter activity is significantly induced by 24-h treatment with Nic (10 μM) or E2 (10 nM) (>1.8 and ~2.3-fold, respectively) in MCF-7 cells. Pretreatment with EGCG eliminated the Nic- and E2-induced α9-nAChR promoter-dependent luciferase activity. We further demonstrate that combined treatment with EGCG profoundly inhibits [3H]-Nic/ α9-nAChR binding activity in breast cancer cells. Conclusions: We found that the EGCG could be used as an agent for blocking smoking (Nic)- or hormone (E2)-induced breast cancer cell proliferation by inhibiting of α9-nAChR signaling pathway. This study reveals the novel antitumor mechanisms of EGCG, and these results may have significant applications for chemopreventive purposes in human breast cancer.

Original languageEnglish
Pages (from-to)455-466
Number of pages12
JournalMolecular Nutrition and Food Research
Volume55
Issue number3
DOIs
Publication statusPublished - Mar 2011

Fingerprint

cholinergic receptors
nicotine
epigallocatechin
Nicotinic Receptors
Polyphenols
Tea
Nicotine
breast neoplasms
tea
estrogens
polyphenols
Estrogens
Up-Regulation
Breast Neoplasms
promoter regions
MCF-7 Cells
Luciferases
luciferase
Smoking
cell proliferation

Keywords

  • (-)-Epigallocatechin-3-gallate
  • Breast cancer
  • Estradiol
  • Nicotine
  • Nicotinic acetylcholine receptor

ASJC Scopus subject areas

  • Food Science
  • Biotechnology

Cite this

Tea polyphenol (-)-epigallocatechin-3-gallate inhibits nicotine- and estrogen-induced α9-nicotinic acetylcholine receptor upregulation in human breast cancer cells. / Tu, Shih Hsin; Ku, Chung Yu; Ho, Chi Tang; Chen, Ching Shyang; Huang, Ching Shui; Lee, Chia Hwa; Chen, Li Ching; Pan, Min Hsiung; Chang, Hui Wen; Chang, Chien Hsi; Chang, Yu Jia; Wei, Po Li; Wu, Chih Hsiung; Ho, Yuan Soon.

In: Molecular Nutrition and Food Research, Vol. 55, No. 3, 03.2011, p. 455-466.

Research output: Contribution to journalArticle

Tu, Shih Hsin ; Ku, Chung Yu ; Ho, Chi Tang ; Chen, Ching Shyang ; Huang, Ching Shui ; Lee, Chia Hwa ; Chen, Li Ching ; Pan, Min Hsiung ; Chang, Hui Wen ; Chang, Chien Hsi ; Chang, Yu Jia ; Wei, Po Li ; Wu, Chih Hsiung ; Ho, Yuan Soon. / Tea polyphenol (-)-epigallocatechin-3-gallate inhibits nicotine- and estrogen-induced α9-nicotinic acetylcholine receptor upregulation in human breast cancer cells. In: Molecular Nutrition and Food Research. 2011 ; Vol. 55, No. 3. pp. 455-466.
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abstract = "Scope: The aim of this research was to explore whether the tea-polyphenol (-)-epigallocatechin-3-gallate (EGCG) could be used as a potential agent for blocking smoking (nicotine, Nic)- or hormone (estradiol, E2)-induced breast cancer cell proliferation through inhibition of a common signaling pathway. Methods and results: To explore whether Nic (>0.1 μM, 24 h) and E2 (>1 nM, 24 h) significantly increased α9-nicotinic acetylcholine (α9-nicotinic acetylcholine receptor (nAChR)) mRNA and protein expression levels, real-time PCR and immunoblotting analysis experiments were performed in human breast cancer (MCF-7) cells. Luciferase promoter activity experiment was performed to test the α9-nAChR promoter activity affected by Nic, E2 or EGCG. The results indicate that treatment with EGCG (1 μM) profoundly decreases Nic- and E2-induced MCF-7 proliferation by down regulating α9-nAChR expression. The α9-nAChR promoter activity is significantly induced by 24-h treatment with Nic (10 μM) or E2 (10 nM) (>1.8 and ~2.3-fold, respectively) in MCF-7 cells. Pretreatment with EGCG eliminated the Nic- and E2-induced α9-nAChR promoter-dependent luciferase activity. We further demonstrate that combined treatment with EGCG profoundly inhibits [3H]-Nic/ α9-nAChR binding activity in breast cancer cells. Conclusions: We found that the EGCG could be used as an agent for blocking smoking (Nic)- or hormone (E2)-induced breast cancer cell proliferation by inhibiting of α9-nAChR signaling pathway. This study reveals the novel antitumor mechanisms of EGCG, and these results may have significant applications for chemopreventive purposes in human breast cancer.",
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AU - Ku, Chung Yu

AU - Ho, Chi Tang

AU - Chen, Ching Shyang

AU - Huang, Ching Shui

AU - Lee, Chia Hwa

AU - Chen, Li Ching

AU - Pan, Min Hsiung

AU - Chang, Hui Wen

AU - Chang, Chien Hsi

AU - Chang, Yu Jia

AU - Wei, Po Li

AU - Wu, Chih Hsiung

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KW - Estradiol

KW - Nicotine

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