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Zanthoxylum fruit extract from Japanese pepper promotes autophagic cell death in cancer cells

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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)

Submitter: 河野 透

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