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    Title: 人類卵巢癌細胞中Chk2蛋白的活化有助於黃芩素所誘導之G2M細胞週期停滯
    Other Titles: Activation of Chk2 contributes to baicalein-induced G2/M cell cycle arrest in human ovarian cancer cells
    Authors: 邵韋勳;Shao, Wei-Syun
    Contributors: 淡江大學化學學系碩士班
    莊子超;Chuang, Tzu-Chao
    Keywords: 細胞檢查點激酶;細胞週期;黃芩素;Chk2;G2/M arrest;Baicalein
    Date: 2011
    Issue Date: 2011-12-28 18:10:01 (UTC+8)
    Abstract: 類黃酮化合物是一種天然多酚類化合物,其持續攝取已經是被證實是可以促進身體健康、預防疾病產生以及防止癌症生成。在本研究中我們評估了類黃酮化合物-黃芩素 (Baicalein) 在人類卵巢癌的抗癌效果。經由實驗結果發現,在黃芩素的作用下,無論是隨著藥物作用濃度的提升或者是隨著作用時間的拉長,都會使得人類卵巢癌細胞之細胞生長能力受到明顯的抑制。然而,這些卵巢癌細胞在黃芩素作用下所導致的細胞生長抑制效果,是透過細胞週期 G2/M 停滯所造成。另外,經由實驗結果發現,黃芩素能夠誘導卵巢癌細胞內活性氧化物質 (ROS) 的生成量增加、H2AX 蛋白磷酸化和 Chk2蛋白的活化。除此之外,一些細胞週期 G2/M 的調控蛋白,如:Cdc25C、 Cdk1 以及 cyclin B1之蛋白質表現量也會在黃芩素的作用下而明顯下滑。綜合以上結果,人類卵巢癌細胞在黃芩素作用下所造成的細胞週期 G2/M 停滯現象,可能是由於 ROS 所導致的 DNA 受損而引發。
    Baicalein has been reported to exhibit anti-tumor activities. In this study, we examined the anti-proliferating effects of baicalein on ovarian cancer cells. We found that baicalein inhibited the cell growth of ovarian cancer cells. Besides, our results demonstrate that baicalein caused reactive oxygen species (ROS) generation, H2AX phosphorylation and Chk2 activation in ovarian cancer cells. Furthermore, we also observed that G2/M regulatory molecules such as Cdc25C, Cdk1, cyclin B1 were down-regulation by baicalein. Taken together, these data suggest baicalein may generate ROS to cause DNA damage and then results in G2/M arrest in ovarian cancer cells.
    Appears in Collections:[化學學系暨研究所] 學位論文

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