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歷 年 稿 件 內 容
 
*類別： D組-分子醫學
* 姓名： 何杏棻
投稿種類： 壁報
*中文投稿標題： 丹參酮IIA調升死亡受器而提升標靶藥TRAIL之抑癌效能
*中文作者姓名列： 何杏棻, 林君謚
*中文服務單位： 中臺科技大學醫學檢驗生物技術系
*英文投稿標題： Tanshinone IIA facilitates TRAIL sensitization through CHOP-mediated DR5 up-regulation in human ovarian cancer cells
*英文作者姓名列： Tsing-Fen Ho, Jyun-Yi Lin
*英文服務單位： Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung, Taiwan
* 投稿摘要： Tanshinone IIA (TIIA) extracted from Salvia miltiorrhiza has been shown to possess antitumor and TRAIL-sensitizing activity. The involvement of DR5 in the mechanism whereby TIIA exerts its effects is unknown. This study aimed to explore the mechanism underlying TIIA augmentation of TRAIL-induced cell death in ovarian carcinoma cells. Cell viability was determined by MTS assay. Real-time RT-PCR and Western blotting were used to assess the mRNA and protein expression of relating signaling proteins. Transcriptional activation was explored by dual-luciferase reporter assay. We found that TIIA sensitized human ovarian carcinoma cells to TRAIL-induced extrinsic apoptosis. Combined treatment with subtoxic concentrations of TIIA and TRAIL was more effective than single treatments with respect to cytotoxicity, clonogenic inhibition, and the induction of caspase-8 and PARP activity in ovarian carcinoma cell lines TOV-21G and SKOV3. TIIA induced DR5 protein and mRNA expression in a concentration-dependent manner. DR5/Fc treatment markedly suppressed the TRAIL cytotoxicity enhanced by TIIA. These results indicate that DR5 plays an essential role in TIIA-induced TRAIL sensitization and that induction of DR5 by TIIA is mediated through up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP). Knockdown of CHOP gene expression by shRNA attenuated DR5 up-regulation and rescued cell viability under the treatment of TIIA-TRAIL combination. TIIA promoted JNK-mediated signaling to up-regulated CHOP and thereby inducing DR5 expression as shown by the ability of a JNK inhibitor potently suppressed the TIIA-mediated activation of CHOP and DR5. In addition, the quenching of ROS using NAC prevented induction of JNK phosphorylation and CHOP induction. Furthermore, inhibition of ROS by NAC significantly attenuated TRAIL sensitization by TIIA. Taken together, these data suggest that TIIA enhances TRAIL-induced apoptosis by upregulating DR5 receptors through the ROS-JNK-CHOP signaling axis in human ovarian carcinoma cells.
*關鍵字1 ： Tanshinone IIA
*關鍵字2 ： TRAIL
*關鍵字3 ： DR5
*關鍵字4 ： ROS
*關鍵字5 ： CHOP
* 服務機關：
* 第一作者： 何杏棻
* 身分字號： *****07700
其他投稿作者： 林君謚
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審查委員意見： 建議入選
審查委員意見： OK
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