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Tea Extracts Confer Its Antiproliferating Effects Through Inhibition of Nicotine- and Estrogen-induced 9-Nicotinic Acetylcholine Receptor Upregulation in Human Breast Cancer Cells

We have previously demonstrated that the tea-polyphenol (-)-epigallocatechin-3-gallate (EGCG) could be used as an agent for blocking smoking (nicotine, Nic)- or hormone (estradiol, E2)-induced breast cancer cell proliferation by inhibiting a common signaling pathway. We found that Nic (>0.1 μM, 24 h) and E2 (>1 nM, 24 h) significantly increased α9-nicotinic acetylcholine (α9-nAChR) mRNA and protein expression levels in human breast cancer (MCF-7) cells. We then hypothesized that green tea and black tea-extract ingredients (TEIs) with inhibitory effects on α9-nAChR protein levels could be used to block the Nic- or E2-mediated carcinogenic signals. Our previous results indicated that treatment with EGCG (1 μM) profoundly decreased Nic- and E2-induced MCF-7 proliferation by down regulating α9-nAChR expression. In addition, our previous study, using a luciferase promoter activity experiment, demonstrated that α9-nAChR promoter activity was 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 demonstrated that treatment with TEIs (10 μg/mL) profoundly inhibited α9-nAChR proteins level when compared with EGCG-treatment alone in breast cancer cells. This study reveals the novel antitumor mechanisms of TEI, and these results may have significant applications for chemopreventive purposes in human breast cancer.

Publication details

https://doi.org/10.1039/9781849737685-00256
Print publication date
13 Mar 2013
Copyright year
2013
Print ISBN
978-1-84973-644-2
PDF eISBN
978-1-84973-768-5
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