CTAB induced mitochondrial apoptosis by activating the AMPK–p53 pathway in hepatocarcinoma cells | Zendy

Yue Pan | Zendy; Zheng Wang | Zendy; Dan Shao | Zendy; Huilin Zheng | Zendy; Yujing Chen | Zendy; Xiao Zheng | Zendy; Ming Zhang | Zendy; Jing Li | Zendy; Feng Li | Zendy; Li Chen | Zendy

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CTAB induced mitochondrial apoptosis by activating the AMPK–p53 pathway in hepatocarcinoma cells

Author(s) -

Yue Pan,

Zheng Wang,

Dan Shao,

Huilin Zheng,

Yujing Chen,

Xiao Zheng,

Ming Zhang,

Jing Li,

Feng Li,

Li Chen

Publication year - 2015

Publication title -

toxicology research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.709

H-Index - 31

eISSN - 2045-4538

pISSN - 2045-452X

DOI - 10.1039/c4tx00227j

Subject(s) - ampk , apoptosis , microbiology and biotechnology , chemistry , mitochondrion , cancer research , biology , biochemistry , phosphorylation , protein kinase a

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.

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