Chrysophanol induces necrosis through the production of ROS and alteration of ATP levels in J5 human liver cancer cells |
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| Authors: | Chi‐Cheng Lu Jai‐Sing Yang An‐Cheng Huang Te‐Chun Hsia Su‐Tze Chou Chao‐Lin Kuo Hsu‐Feng Lu Tsung‐Han Lee Wellington G Wood Jing‐Gung Chung |
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| Affiliation: | 1. Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan;2. Department of Pharmacology, China Medical University, Taichung, Taiwan;3. Department of Nursing, St. Mary's Medicine Nursing and Management College, Yilan, Taiwan;4. Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan;5. Department of Food and Nutrition, Providence University, Salu, Taichung, Taiwan;6. School of Chinese Medicine Resources, China Medical University, Taichung, Taiwan;7. Department of Clinical Pathology, Cheng Hsin Rehabilitation Medical Center, Taipei, Taiwan;8. Department of Pharmacology, University of Minnesota, School of Medicine and Geriatric Research, Education and Clinical Center, VA Medical Center, Minneapolis, MN, USA;9. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan;10. Department of Biotechnology, Asia University, Wufeng, Taichung, Taiwan |
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| Abstract: | Anthraquinone compounds have been shown to induce apoptosis in different cancer cell types. Effects of chrysophanol, an anthraquinone compound, on cancer cell death have not been well studied. The goal of this study was to examine if chrysophanol had cytotoxic effects and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose‐ and time‐dependent manner. Non‐apoptotic cell death was induced by chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption. Blockage of apoptotic induction by a general caspase inhibitor (z‐VAD‐fmk) failed to protect cells against chrysophanol‐induced cell death. The levels of reactive oxygen species production and loss of mitochondrial membrane potential (ΔΨm) were also determined to assess the effects of chrysophanol. However, reductions in adenosine triphosphate levels and increases in lactate dehydrogenase activity indicated that chrysophanol stimulated necrotic cell death. In summary, human liver cancer cells treated with chrysophanol exhibited a cellular pattern associated with necrosis and not apoptosis. |
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| Keywords: | Adenosine triphosphate Chrysophanol J5 human liver cancer cells Necrosis Reactive oxygen species |
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