大黄素 增强顺铂引起的 细胞毒性 通过下调ERCC1与ERK1 2的失活.pdf

Lung Cancer 69 (2010) 155–164 Contents lists available at ScienceDirect Lung Cancer j o u rn al h omepage: w w w. elsev /locate/lung can Emodin enhances cisplatin-induced cytotoxicity via down-regulation of ERCC1 and inactivation of ERK1/2 Jen-Chung Ko a , Ying-Jhen Su b , Szu-Ting Lin b , Jhih-Yuan Jhan b , Shih-Ci Ciou b , Chao-Min Cheng b , Yu-Fan Chiu b , Ya-Hsun Kuo b , Min-Shao Tsai b , Yun-Wei Lin b,∗ a Department of Internal Medicine, Hsinchu Hospital, Department of Health, The Executive Yuan, Taiwan b Molecular Oncology Laboratory, Department of Biochemical Science and Technology, National Chiayi University, No. 300 Syuefu Rd., Chiayi City 60004, Taiwan a r t i c l e i n f o a b s t r a c t Article history: Emodin, a tyrosine kinase inhibitor, is a natural anthraquinone derivative found in the roots and rhi- Received 2 September 2009 zomes of numerous plants; it exhibits an anticancer effect on many malignancies. The most important Received in revised form 22 October 2009 chemotherapeutic agent for patients with advanced non-small cell lung cancer (NSCLC) is a platinum- Accepted 26 October 2009 containing compound such as cisplatin or carboplatin. The molecular mechanism underlying decreased NSCLC cell viability after treatment with emodin and cisplatin is unclear. Therefore, the aim of this Keywords: study was to assess the cytotoxic effect of combined emodin and cisplatin on NSCLC cell lines and ER