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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)
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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MDPI and ACS Style

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. https://doi.org/10.3390/ijms19051309

AMA Style

Woo SM, Seo SU, Min K-j, Im S-S, Nam J-O, Chang J-S, Kim S, Park J-W, Kwon TK. Corosolic Acid Induces Non-Apoptotic Cell Death through Generation of Lipid Reactive Oxygen Species Production in Human Renal Carcinoma Caki Cells. International Journal of Molecular Sciences. 2018; 19(5):1309. https://doi.org/10.3390/ijms19051309

Chicago/Turabian Style

Woo, Seon Min, Seung Un Seo, Kyoung-jin Min, Seung-Soon Im, Ju-Ock Nam, Jong-Soo Chang, Shin Kim, Jong-Wook Park, and Taeg Kyu Kwon. 2018. "Corosolic Acid Induces Non-Apoptotic Cell Death through Generation of Lipid Reactive Oxygen Species Production in Human Renal Carcinoma Caki Cells" International Journal of Molecular Sciences 19, no. 5: 1309. https://doi.org/10.3390/ijms19051309

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