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Corosolic Acid Induces Non-Apoptotic Cell Death through Generation of Lipid Reactive Oxygen Species Production in Human Renal Carcinoma Caki Cells

1
Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea
2
Physiology of Department, School of Medicine, Keimyung University, Daegu 42601, Korea
3
Department of Food Science and Biotechnology, Kyungpook National University, Daegu 41566, Korea
4
Department of Life Science, College of Science and Technology, Daejin University, Kyeonggido 11159, Korea
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(5), 1309; https://doi.org/10.3390/ijms19051309
Received: 30 March 2018 / Revised: 20 April 2018 / Accepted: 24 April 2018 / Published: 27 April 2018
(This article belongs to the Section Biochemistry)
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Abstract

Corosolic acid is one of the pentacyclic triterpenoids isolated from Lagerstroemia speciose and has been reported to exhibit anti-cancer and anti-proliferative activities in various cancer cells. In the present study, we investigated the molecular mechanisms of corosolic acid in cancer cell death. Corosolic acid induces a decrease of cell viability and an increase of cell cytotoxicity in human renal carcinoma Caki cells. Corosolic acid-induced cell death is not inhibited by apoptosis inhibitor (z-VAD-fmk, a pan-caspase inhibitor), necroptosis inhibitor (necrostatin-1), or ferroptosis inhibitors (ferrostatin-1 and deferoxamine (DFO)). Furthermore, corosolic acid significantly induces reactive oxygen species (ROS) levels, but antioxidants (N-acetyl-l-cysteine (NAC) and trolox) do not inhibit corosolic acid-induced cell death. Interestingly, corosolic acid induces lipid oxidation, and α-tocopherol markedly prevents corosolic acid-induced lipid peroxidation and cell death. Anti-chemotherapeutic effects of α-tocopherol are dependent on inhibition of lipid oxidation rather than inhibition of ROS production. In addition, corosolic acid induces non-apoptotic cell death in other renal cancer (ACHN and A498), breast cancer (MDA-MB231), and hepatocellular carcinoma (SK-Hep1 and Huh7) cells, and α-tocopherol markedly inhibits corosolic acid-induced cell death. Therefore, our results suggest that corosolic acid induces non-apoptotic cell death in cancer cells through the increase of lipid peroxidation. View Full-Text
Keywords: corosolic acid; non-apoptotic cell death; α-tocopherol; lipid ROS corosolic acid; non-apoptotic cell death; α-tocopherol; lipid ROS
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Woo, S.M.; Seo, S.U.; Min, K.-J.; Im, S.-S.; Nam, J.-O.; Chang, J.-S.; Kim, S.; Park, J.-W.; Kwon, T.K. Corosolic Acid Induces Non-Apoptotic Cell Death through Generation of Lipid Reactive Oxygen Species Production in Human Renal Carcinoma Caki Cells. Int. J. Mol. Sci. 2018, 19, 1309.

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