Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 99, Issue -, Pages 1-8Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2016.11.008
Keywords
Naringenin; Pancreatic cancer; Peroxiredoxin-1; Reactive oxygen species; Apoptosis signal-regulation kinase 1
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Funding
- Basic Science Research Program through the National Research Foundation of Korea - Ministry of Education, Science and Technology [NRF-2013R1A1A2A10011594]
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Naringenin, one of the most abundant flavonoids in natural citrus fruits, has been investigated for its ability to inhibit growth of breast, colon, gastric and prostate cancer cells. However, naringenin-induced cell death in pancreatic cancer is not well understood. Therefore, we analyzed the naringenin-induced apoptosis mechanism using human pancreatic cancer SNU-213 cells. Annexin V+/PI + marked cells increased from 5.10% to 8.29%, 25.06% and 35.31% in response to treatment with 200, 400, and 600 mu M naringenin, respectively. Two-dimensional electrophoresis to identify possible target-related proteins of naringenin-induced apoptosis revealed seven proteins. Among these, the expression of peroxiredoxin-1 (Prdx-1), which modulates redox homeostasis of cells, was decreased. To obtain a broad understanding of the interactive mechanism of naringenin and Prdx-1, we observed changes in reactive oxygen species (ROS) in naringenin-treated SNU-213 cells. The ROS levels were 130.02 +/- 20.21%, 182.04 +/- 5.39%, and 237.21 +/- 12.71% in response to 200, 400, and 600 mu M naringenin treatment, respectively. Increases in ROS were followed by up-regulation of apoptosis signal-regulation kinase 1 (ASK1). Moreover, the JNK, p38 and p53 proteins were upregulated. Overall, the results of this study suggest that naringenin causes ASK1-induced apoptosis mediated by ROS. (C) 2016 Elsevier Ltd. All rights reserved.
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