CTAB induced mitochondrial apoptosis by activating the AMPK-p53 pathway in hepatocarcinoma cells
CTAB induced mitochondrial apoptosis by activating the AMPK-p53 pathway in hepatocarcinoma cells
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CTAB通过激活AMPK-p53通路诱导肝癌细胞线粒体凋亡
DOI：
10.1039/c4tx00227j
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发表时间：
2015
影响因子：
2.1
通讯作者：
Chen Li
中科院分区：
文献类型：
--
作者：
Pan Yue;Wang Zheng;Shao Dan;Zheng Huilin;Chen Yujing;Zheng Xiao;Zhang Ming;Li Jing;Li Feng;Chen Li
能量代谢的重新编程作为一个新的概念正在出现，是癌症的标志之一。CTAB是一种具有抑制线粒体H-ATP合成酶活性的季铵化合物，对细胞能量代谢具有潜在的影响。本研究探讨了CTAB对肝癌细胞的作用及其机制。结果表明，CTAB以剂量和时间依赖的方式降低各种肝癌细胞的细胞活力。结果表明，CTAB通过激活AMPK和p53信号通路诱导人肝癌HepG 2细胞线粒体凋亡。我们的研究揭示了CTAB作为一个有前途的癌症治疗候选人。
The reprogramming of energy metabolism as a new concept is emerging and is one of the hallmarks of cancer. CTAB, known as a quaternary ammonium compound with the activity of inhibiting mitochondrial H-ATP synthase, has shown the potential to influence cell energy metabolism. In this study, we investigated the effects and the underlying mechanisms of CTAB on liver cancer cells. The results showed that CTAB reduced the cell viability of various hepatocarcinoma cells in a dose- and time-dependent manner. The results showed that CTAB induced mitochondrial apoptosis in human hepatocarcinoma HepG2 cells by activating AMPK and p53 signaling pathways. Our study sheds light on CTAB as a promising cancer therapeutic candidate.