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歷 年 稿 件 內 容
 
*類別：
* 姓名： 鄧豪恩
投稿種類： 壁報
*中文投稿標題： 山竹萃取物(garcinol)在抽菸所誘發人類乳癌細胞之抗癌機制探討
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* 投稿摘要： Previous studies have demonstrated that the persistent exposure of human bronchial epithelial cells to nicotine (Nic) through nicotinic acetylcholine receptors increases cyclin D1 promoter activity and protein expression. The main purpose of this study was to elucidate the carcinogenic role of cyclin D3, which is involved in breast tumorigenesis when induced by Nic. Real-time PCR analysis revealed that cyclin D3 is highly expressed at the mRNA level in surgically dissected breast tumor tissue compared to the surrounding normal tissue (Tumor/Normal fold ratio = 17.93, n = 74). To test whether Nic/nicotinic acetylcholine receptor (nAChR) binding could affect cyclin D3 expression in human breast cancer cells, two transformed cell lines (MCF-10A-Nic and MCF-10A-NNK) were generated from normal breast epithelial cells (MCF-10A) with inducible α9-nAChR gene expression using the adenovirus tetracycline-regulated Tet-off system. Tet-regulated overexpression of 9-nAChR in MCF-10A-Nic xenografted BALB/c-nu/nu mice resulted in a significant induction of cyclin D3. In contrast, cyclin D3 expression was down-regulated in 9-nAChR knock-down (siRNA) MDA-MB-231-xenografted tumors in NOD.CB17-PRKDC(SCID)/J(NOD-SCID) mice. Furthermore, we found that Nic-induced human breast cancer (MDA-MB-231) cell proliferation was inhibited by garcinol (Gar; 1 M), isolated from edible fruit Garcinia indica, through down-regulation of 9-nAChR and cyclin D3 expression. These results suggest that 9-nAChR-mediated cyclin D3 overexpression is important for nicotine-induced transformation of normal human breast epithelial cells. The homeostatic regulation of cyclin D3 has potential as a molecular target for antitumor chemotherapeutic or chemopreventive purposes in clinical breast cancer patients.
*關鍵字1 ： cyclin D3 proteins
*關鍵字2 ： nicotinic receptor
*關鍵字3 ： human breast cancer
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* 第一作者： 鄧豪恩
* 身分字號： *****10336
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審查委員意見： 無特殊意見。單位:Texhnology->Technology
審查委員意見： ok
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