Studies on the Potential Molecular Mechanisms of Nicotinic Receptors-mediated Carcinogenic Effects in Human Breast Cancer Cells

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Title:	Studies on the Potential Molecular Mechanisms of Nicotinic Receptors-mediated Carcinogenic Effects in Human Breast Cancer Cells
Authors:	吳志雄 Wu CH;Ho YS
Contributors:	外科學科
Date:	2008
Issue Date:	2009-08-13 14:46:31 (UTC+8)
Abstract:	Tobacco-smoking is one of the well understanding carcinogenic factors involved in breast cancer formation. In this study, we first demonstrated that the several types of nicotinic acetylcholine receptors (nAchRs) were detected in breast cancer cell lines including MCF-7 and MDA-MB-231. The expression of the nAchR mRNA levels in tumor tissues from 157 cases of breast cancer patients in Taiwan were determined and found that the α5, α9 and α10 subunits of the nAchRs were the most prevalence in both normal and tumor tissue. Quantitative assays of the nAchRs mRNA levels was performed by real-time PCR analysis which revealed that the expression levels of 9-nAchR was higher in most of the tumor tissue when compared to the normal tissues which dissected form the tumor margin. The receptor binding activity assay was performed and demonstrated that 9-nAchR significant binding to its ligand (nicotine) in a concentration as low as 7 M and reached the maximal level as soon as 60 minutes. The 9-nAchR expression in breast cancer cells was knock-downed by SiRNA technique and demonstrated that Akt-p (ser473) signaling regulatory pathways play an important role in nicotine-mediated breast cancer cells proliferation. We further demonstrated that the -9-nAchR expression was significant upregulated in the promoter level by nicotine and sex hormone (estradiol, E2) as evidenced by luciferase reporter assay. Our results further demonstrated that E2-mediated nAchR expression was through activation of the estrogen receptor (ER) as demonstrated by chromatin immunoprecipitation analysis. In vivo study was performed by nude mice model and demonstrated that the 9- nAchR-mediated cancer cell proliferation may play a major role in response to nicotine-induced breast tumor formation. Such results implied that 9-nAchR and its cooperative role with sex hormone (such as E2) may be significant in nicotine-mediated breast tumor carcinogenesis
Relation:	BIT Life Sciences 1st Annual World Cancer Congress 2008, Shanghai, China
Data Type:	conference
Appears in Collections:	[Department of Surgery] Conference Paper

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