NDLI: The quinone-based derivative, HMNQ induces apoptotic and autophagic cell death by modulating reactive oxygen species in cancer cells.

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The quinone-based derivative, HMNQ induces apoptotic and autophagic cell death by modulating reactive oxygen species in cancer cells.

Content Provider	Europe PMC
Author	Lee, Eun Byul Cheon, Min Gyeong Cui, Jun Lee, Yoo Jin Seo, Eun Kyoung Jang, Ho Hee
Copyright Year	2017
Abstract	8-Hydroxy-2-methoxy-1,4-naphthoquinone (HMNQ), a natural compound isolated from the bark of Juglans sinensis Dode, displays cytotoxic activity against various human cancer cells. However, the molecular mechanism of the anticancer effect is unclear. In this study, we examined the cytotoxic mechanism of HMNQ at the molecular level in human cancer cells. Cells were treated with HMNQ in a dose- or time-dependent manner. HMNQ treatment inhibited cell viability, colony formation and cell migration, indicating that HMNQ induced cancer cell death. HMNQ-treated cells resulted in apoptotic cell death through PARP-1 cleavage, Bax upregulation and Bcl-2 downregulation. HMNQ was also observed to induce autophagy by upregulating Beclin-1 and LC3. Furthermore, HMNQ induced reactive oxygen species (ROS) production, which was attenuated by the ROS scavengers, NAC and GSH. Finally, HMNQ increased expression of JNK phosphorylation and the JNK inhibitor SP600125 rescued HMNQ-induced cell death, suggesting that the cytotoxicity of HMNQ is mediated by the JNK signaling pathway. Taken together, our findings show that HMNQ exhibits anticancer activity through induction of ROS-mediated apoptosis and autophagy in human cancer cells. These data suggest the potential value of HMNQ as a natural anticancer drug.
Journal	Oncotarget
Volume Number	8
PubMed Central reference number	PMC5725121
Issue Number	59
PubMed reference number	29245930
e-ISSN	19492553
DOI	10.18632/oncotarget.21005
Language	English
Publisher	Impact Journals LLC
Publisher Date	2017-09-18
Access Restriction	Open
Rights License	This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Copyright: © 2017 Lee et al.
Subject Keyword	anticancer drug natural compound reactive oxygen species (ROS) apoptosis autophagy
Content Type	Text
Resource Type	Article
Subject	Oncology

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