Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 김희선 | * |
dc.date.accessioned | 2016-08-28T10:08:32Z | - |
dc.date.available | 2016-08-28T10:08:32Z | - |
dc.date.issued | 2013 | * |
dc.identifier.issn | 2041-4889 | * |
dc.identifier.other | OAK-10464 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/224052 | - |
dc.description.abstract | Compound K (20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol) is an active metabolite of ginsenosides and induces apoptosis in various types of cancer cells. This study investigated the role of autophagy in compound K-induced cell death of human HCT-116 colon cancer cells. Compound K activated an autophagy pathway characterized by the accumulation of vesicles, the increased positive acridine orange-stained cells, the accumulation of LC3-II, and the elevation of autophagic flux. Whereas blockade of compound K-induced autophagy by 3-methyladenein and bafilomycin A1 significantly increased cell viability. In addition, compound K augmented the time-dependent expression of the autophagy-related proteins Atg5, Atg6, and Atg7. However, knockdown of Atg5, Atg6, and Atg7 markedly inhibited the detrimental impact of compound K on LC3-II accumulation and cell vitality. Compound K-provoked autophagy was also linked to the generation of intracellular reactive oxygen species (ROS); both of these processes were mitigated by the pre-treatment of cells with the antioxidant N-acetylcysteine. Moreover, compound K activated the c-Jun NH2-terminal kinase (JNK) signaling pathway, whereas downregulation of JNK by its specific inhibitor SP600125 or by small interfering RNA against JNK attenuated autophagy-mediated cell death in response to compound K. Compound K also provoked apoptosis, as evidenced by an increased number of apoptotic bodies and sub-G1 hypodiploid cells, enhanced activation of caspase-3 and caspase-9, and modulation of Bcl-2 and Bcl-2-associated X protein expression. Notably, compound K-stimulated autophagy as well as apoptosis was induced by disrupting the interaction between Atg6 and Bcl-2. Taken together, these results indicate that the induction of autophagy and apoptosis by compound K is mediated through ROS generation and JNK activation in human colon cancer cells. © 2013 Macmillan Publishers Limited All rights reserved. | * |
dc.language | English | * |
dc.title | A ginseng metabolite, compound K, induces autophagy and apoptosis via generation of reactive oxygen species and activation of JNK in human colon cancer cells | * |
dc.type | Article | * |
dc.relation.issue | 8 | * |
dc.relation.volume | 4 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Cell Death and Disease | * |
dc.identifier.doi | 10.1038/cddis.2013.273 | * |
dc.identifier.wosid | WOS:000324146000007 | * |
dc.identifier.scopusid | 2-s2.0-84882658193 | * |
dc.author.google | Kim A.D. | * |
dc.author.google | Kang K.A. | * |
dc.author.google | Kim H.S. | * |
dc.author.google | Kim D.H. | * |
dc.author.google | Choi Y.H. | * |
dc.author.google | Lee S.J. | * |
dc.author.google | Hyun J.W. | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.date.modifydate | 20240118140922 | * |