五乙酰京尼平苷诱导的C6胶质瘤细胞凋亡与蛋白激酶C-δ的激活有关。
Penta-acetyl geniposide-induced C6 glioma cell apoptosis was associated with the activation of protein kinase C-delta.
作者信息
Peng Chiung-Huei, Tseng Tsui-Hwa, Liu Jer-Yuh, Hsieh Yi-Hsien, Huang Chien-Ning, Hsu Shu-Ping, Wang Chau-Jong
机构信息
Institute of Biochemistry, Chung Shan Medical University, No. 110, Section 2, Chien Kuo N. Road, Taichung 402, Taichung, Taiwan, ROC.
出版信息
Chem Biol Interact. 2004 Apr 15;147(3):287-96. doi: 10.1016/j.cbi.2004.01.003.
Herbal medicine has been utilized to treat a variety of diseases, including cancer. On the other hand, disturbance of apoptosis is often observed in cancer cells. It has been reported that protein kinase C (PKC) isoforms are involved in the signaling of apoptosis. In the present study, we investigate the antitumor effect and possible mechanism of a herbal-originated product, (Ac)(5)GP. We demonstrate that (Ac)(5)GP treatment results in DNA fragmentation of C6 glioma cells dose-dependently. Stimulated by (Ac)(5)GP, PKCdelta and PKCzeta were activated and translocated to the cell membrane fraction. Flow cytometry analysis showed that PKCdelta, but not PKCzeta inhibition blocks the (Ac)(5)GP-induced apoptosis by decreasing the cell population of sub G1 peak. However, the mRNA levels of PKCdelta and PKCzeta were not altered by (Ac)(5)GP-induced glioma cell apoptosis. These results suggested that the treatment of (Ac)(5)GP induces apoptosis of tumor cells through the activation but not the synthesis of PKCdelta.
草药已被用于治疗包括癌症在内的多种疾病。另一方面，癌细胞中常观察到细胞凋亡紊乱。据报道，蛋白激酶C（PKC）亚型参与细胞凋亡信号传导。在本研究中，我们研究了一种源自草药的产品（Ac）5GP的抗肿瘤作用及其可能机制。我们证明（Ac）5GP处理可剂量依赖性地导致C6胶质瘤细胞DNA片段化。在（Ac）5GP刺激下，PKCδ和PKCζ被激活并转位至细胞膜组分。流式细胞术分析表明，PKCδ抑制而非PKCζ抑制可通过减少亚G1峰细胞群来阻断（Ac）5GP诱导的细胞凋亡。然而，（Ac）5GP诱导的胶质瘤细胞凋亡并未改变PKCδ和PKCζ的mRNA水平。这些结果表明，（Ac）5GP处理通过激活而非合成PKCδ诱导肿瘤细胞凋亡。
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