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Zanthoxylum fruit extract from Japanese pepper promotes autophagic cell death in cancer cells
This item is licensed under:Creative Commons Attribution 3.0 Unported
| Title: | Zanthoxylum fruit extract from Japanese pepper promotes autophagic cell death in cancer cells |
| Authors: | Nozaki, Reo Browse this author | | Kono, Toru Browse this author →KAKEN DB | | Bochimoto, Hiroki Browse this author →KAKEN DB | | Watanabe, Tsuyoshi Browse this author →KAKEN DB | | Oketani, Kaori Browse this author | | Sakamaki, Yuichi Browse this author | | Okubo, Naoto Browse this author →KAKEN DB | | Nakagawa, Koji Browse this author →KAKEN DB | | Takeda, Hiroshi Browse this author →KAKEN DB |
| Keywords: | autophagy | | autophagic cell death | | vacuolization | | colon cancer | | zanthoxylum fruit |
| Issue Date: | 26-Oct-2016 |
| Publisher: | Impact Journals |
| Journal Title: | Oncotarget |
| Volume: | 7 |
| Issue: | 43 |
| Start Page: | 70437 |
| End Page: | 70446 |
| Publisher DOI: | 10.18632/oncotarget.11926 |
| Abstract: | Zanthoxylum fruit, obtained from the Japanese pepper plant (Zanthoxylum piperitum De Candolle), and its extract (Zanthoxylum fruit extract, ZFE) have multiple physiological activities (e.g., antiviral activity). However, the potential anticancer activity of ZFE has not been fully examined. In this study, we investigated the ability of ZFE to induce autophagic cell death (ACD). ZFE caused remarkable autophagy-like cytoplasmic vacuolization, inhibited cell proliferation, and ultimately induced cell death in the human cancer cell lines DLD-1, HepG2, and Caco-2, but not in A549, MCF7, or WiDr cells. ZFE increased the level of LC3-II protein, a marker of autophagy. Knockdown of ATG5 using siRNA inhibited ZFE-induced cytoplasmic vacuolization and cell death. Moreover, in cancer cells that could be induced to undergo cell death by ZFE, the extract increased the phosphorylation of c-Jun N-terminal kinase (JNK), and the JNK inhibitor SP600125 attenuated both vacuolization and cell death. Based on morphology and expression of marker proteins, ZFE-induced cell death was neither apoptosis nor necrosis. Normal intestinal cells were not affected by ZFE. Taken together, our findings show that ZFE induces JNK-dependent ACD, which appears to be the main mechanism underlying its anticancer activity, suggesting a promising starting point for anticancer drug development. |
| Rights: | http://creativecommons.org/licenses/by/3.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/64034 |
| Appears in Collections: | 薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 河野 透
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