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3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells
The natural, phenolic lipid urushiol exhibits both antioxidant and anticancer activities; however, its biological activity on hepatocellular carcinoma (HCC) has not been previously investigated. Here, we demonstrate that an urushiol derivative, 3-decylcatechol (DC), induces human HCC Huh7 cell death...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601693/ https://www.ncbi.nlm.nih.gov/pubmed/28938597 http://dx.doi.org/10.18632/oncotarget.17732 |
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author | Go, Da-Hye Lee, Yu Geon Lee, Da-Hye Kim, Jin-A Jo, In-Hwa Han, Yeon Soo Jo, Yong Hun Kim, Kwang-Youn Seo, Young-Kyo Moon, Jae-Hak Jung, Chang Hwa Jeon, Tae-Il |
author_facet | Go, Da-Hye Lee, Yu Geon Lee, Da-Hye Kim, Jin-A Jo, In-Hwa Han, Yeon Soo Jo, Yong Hun Kim, Kwang-Youn Seo, Young-Kyo Moon, Jae-Hak Jung, Chang Hwa Jeon, Tae-Il |
author_sort | Go, Da-Hye |
collection | PubMed |
description | The natural, phenolic lipid urushiol exhibits both antioxidant and anticancer activities; however, its biological activity on hepatocellular carcinoma (HCC) has not been previously investigated. Here, we demonstrate that an urushiol derivative, 3-decylcatechol (DC), induces human HCC Huh7 cell death by induction of autophagy. DC initiates the autophagic process by activation of the mammalian target of rapamycin signaling pathway via Unc-51-like autophagy activating kinase 1, leading to autophagosome formation. The autophagy inhibitor, chloroquine, suppressed autolysosome formation and cell death induction by DC, indicating an autophagic cell death. Interestingly, DC also activated the endoplasmic reticulum (ER) stress response that promotes autophagy via p62 transcriptional activation involving the inositol-requiring enzyme 1α/c-Jun N-terminal kinase/c-jun pathway. We also show that cytosolic calcium mobilization is necessary for the ER stress response and autophagy induction by DC. These findings reveal a novel mechanism by which this urushiol derivative induces autophagic cell death in HCC. |
format | Online Article Text |
id | pubmed-5601693 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-56016932017-09-21 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells Go, Da-Hye Lee, Yu Geon Lee, Da-Hye Kim, Jin-A Jo, In-Hwa Han, Yeon Soo Jo, Yong Hun Kim, Kwang-Youn Seo, Young-Kyo Moon, Jae-Hak Jung, Chang Hwa Jeon, Tae-Il Oncotarget Research Paper The natural, phenolic lipid urushiol exhibits both antioxidant and anticancer activities; however, its biological activity on hepatocellular carcinoma (HCC) has not been previously investigated. Here, we demonstrate that an urushiol derivative, 3-decylcatechol (DC), induces human HCC Huh7 cell death by induction of autophagy. DC initiates the autophagic process by activation of the mammalian target of rapamycin signaling pathway via Unc-51-like autophagy activating kinase 1, leading to autophagosome formation. The autophagy inhibitor, chloroquine, suppressed autolysosome formation and cell death induction by DC, indicating an autophagic cell death. Interestingly, DC also activated the endoplasmic reticulum (ER) stress response that promotes autophagy via p62 transcriptional activation involving the inositol-requiring enzyme 1α/c-Jun N-terminal kinase/c-jun pathway. We also show that cytosolic calcium mobilization is necessary for the ER stress response and autophagy induction by DC. These findings reveal a novel mechanism by which this urushiol derivative induces autophagic cell death in HCC. Impact Journals LLC 2017-05-09 /pmc/articles/PMC5601693/ /pubmed/28938597 http://dx.doi.org/10.18632/oncotarget.17732 Text en Copyright: © 2017 Go et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (http://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Go, Da-Hye Lee, Yu Geon Lee, Da-Hye Kim, Jin-A Jo, In-Hwa Han, Yeon Soo Jo, Yong Hun Kim, Kwang-Youn Seo, Young-Kyo Moon, Jae-Hak Jung, Chang Hwa Jeon, Tae-Il 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells |
title | 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells |
title_full | 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells |
title_fullStr | 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells |
title_full_unstemmed | 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells |
title_short | 3-Decylcatechol induces autophagy-mediated cell death through the IRE1α/JNK/p62 in hepatocellular carcinoma cells |
title_sort | 3-decylcatechol induces autophagy-mediated cell death through the ire1α/jnk/p62 in hepatocellular carcinoma cells |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601693/ https://www.ncbi.nlm.nih.gov/pubmed/28938597 http://dx.doi.org/10.18632/oncotarget.17732 |
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