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National Chung Hsing University Institutional Repository - NCHUIR > 生命科學院 > 生物醫學研究所 > 依資料類型分類 > 碩博士論文 >  探討柑橘類黃酮5''-demethylnobiletin在肺癌細胞的抗腫瘤作用

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/152673

標題: 探討柑橘類黃酮5''-demethylnobiletin在肺癌細胞的抗腫瘤作用
Study on the Antitumor Effect of Citrus Flavonoid 5’-Demethylnobiletin in Lung Cancer Cells
作者: 陳欣俞
Chen, Hsing-Yu
Contributors: 林季千
Chi-Chen Lin
生物醫學研究所
關鍵字: 肺癌;G2/M停滯;細胞微管聚合;細胞自噬
G2/M arrest;tubulin polymerization;autophagy;lung cancer
日期: 2013
Issue Date: 2013-11-18 11:04:36 (UTC+8)
Publisher: 生物醫學研究所
摘要: 一般依肺癌的腫瘤特性可以將其分為小細胞肺癌 (small cell lung carcinoma, SCLC) 與非小細胞肺癌 (non-small cell lung carcinoma, NSCLC)。其中,非小細胞肺癌的肺腺癌(adenocarcinoma)又占了肺癌的40%,其預後能力與轉移能力又特別高。川陳皮素(Nobiletin)多存在於柑橘類水果中,屬多甲氧基黃酮(PMF)一類的化合物。5’-去甲基川陳皮素(5’-demethylnobiletin)是從柑橘皮中萃取的天然化合物,目前已有許多文獻指出柑橘類黃酮具有許多生物活性,其中包括了與調控腫瘤相關的路徑(包括:致癌因子的生物活性、細胞訊息傳遞路徑、細胞週期調控與發炎…等等)。在我們的研究中發現5’-去甲基川陳皮素對肺腺癌A549與CL1-5細胞株在24小時會藉由降低cdc25c的表現並且影響細胞微管聚合能力導致影響導致細胞週期滯留在G2/M期,同時發現24小時後開始有細胞自噬的產生,透過活化JNK與Beclin 1誘導細胞自噬,停滯於G2/M期的表現量下降
,因此我們在給予5’-去甲基川陳皮素之前預處理3-甲基腺嘌呤(3-methyladenine)將細胞自噬抑制下來,發現滯留在G2/M期的細胞
表現量增加並且有細胞凋亡的產生。
The main types of lung cancer are small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC). Adenocarcinoma of the lung is a form of non-small cell lung cancer and nearly 40% of lung cancers are adenocarcinoma. Nobiletin is one of polymethoxyflavone (PMF) found in orange peel extract. 5’-demethylnobiletin (DMN) is an auto-hydrolytic product of PMFs from the peel of citrus fruit. Citrus flavonoids have provided evidence for their beneficial action on multiple cancer-related biological pathways (carcinogen bio-activation, cell-signaling, cell cycle regulation and inflammation). In this study, we found that DMN induced G2/M arrest via inhibition of tubulin depolymerization. DMN promote non-small-cell lung carcinoma into mitosis phase via down-regulation of CDC25c and p-cdc2 (tyr 15), but not cyclin B. Then, DMN promote tubulin polymerization induced G2/M arrest. We also found DMN induced autophagy after 24 h by detection of LC3-II expression and autophagy puncta formation in non-small-cell lung carcinoma. In addition, DMN induced JNK phosphorylation in 6 h and activation of Beclin-1 in 12~24 h then decreasing the cell populations of G2/M phase. Therefore, cell pretreated with 3-methyladenine before DMN treatment that reversed the G2/M levels and induced apoptosis in non-small-cell lung carcinoma.
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