Cordycepin induces apoptosis of human ovarian cancer cells by inhibiting CCL5-mediated Akt/NF-kappa B signaling pathway
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Cui, Zhen Yang | - |
dc.contributor.author | Park, Soo Jung | - |
dc.contributor.author | Jo, Eunbi | - |
dc.contributor.author | Hwang, In-Hu | - |
dc.contributor.author | Lee, Kyung-Bok | - |
dc.contributor.author | Kim, Sung-Woo | - |
dc.contributor.author | Kim, Dae Joon | - |
dc.contributor.author | Joo, Jong Chun | - |
dc.contributor.author | Hong, Seok Hoon | - |
dc.contributor.author | Lee, Min-Goo | - |
dc.contributor.author | Jang, Ik-Soon | - |
dc.date.available | 2020-11-02T07:16:10Z | - |
dc.date.issued | 2018-05-23 | - |
dc.identifier.issn | 2058-7716 | - |
dc.identifier.issn | 2058-7716 | - |
dc.identifier.uri | https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/3530 | - |
dc.description.abstract | The chemokine, CCL5, is a key mediator for the recruitment of immune cells into tumors and tissues. Akt/NF-kappa B signaling is significantly activated by CCL5. However, the role of NE-kappa B inactivation in apoptosis induced by negative regulation of CCL5 remains unclear. Here, we analyzed the effect of cordycepin on NE-kappa B activity in SKOV-3 cells and found that cordycepin-mediated inhibition of NE-kappa B signaling induced apoptosis in SKOV-3 cells via the serial activation of caspases. In addition, immune-blotting analysis showed that CCL5 is highly expressed in SKOV-3 cells. In addition to activating caspases, we show that, cordycepin prevents INF-alpha-induced increase in CCL5, Akt, NE-kappa B, and c-FLIPL activation and that CCL5 siRNA could inhibit Akt/NF-kappa B signaling. Moreover, cordycepin negatively regulated the INF-a-mediated IKB/NE-kappa B pathway and c-FLIPL activation to promote JNK phosphorylation, resulting in caspase-3 activation and apoptosis. Also, we show that c-FLIPL is rapidly lost in NE-kappa B activation-deficient. siRNA mediated c-FLIP inhibition increased INK. SP600125, a selective JNK inhibitor, downregulated p-JNK expression in cordycepin-treated SKOV-3 cells, leading to suppression of cordycepin-induced apoptosis. Thus, these results indicate that cordycepin inhibits CCL5-mediated Akt/NF-kappa B signaling, which upregulates caspase-3 activation in SKOV-3 cells, supporting the potential of cordycepin as a therapeutic agent for ovarian cancer. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Cordycepin induces apoptosis of human ovarian cancer cells by inhibiting CCL5-mediated Akt/NF-kappa B signaling pathway | - |
dc.type | Article | - |
dc.publisher.location | 영국 | - |
dc.identifier.doi | 10.1038/s41420-018-0063-4 | - |
dc.identifier.scopusid | 2-s2.0-85051660931 | - |
dc.identifier.wosid | 000463147300002 | - |
dc.identifier.bibliographicCitation | CELL DEATH DISCOVERY, v.4 | - |
dc.citation.title | CELL DEATH DISCOVERY | - |
dc.citation.volume | 4 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | ANTICANCER | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | 3'-DEOXYADENOSINE | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | MIGRATION | - |
dc.subject.keywordPlus | EXTRACT | - |
dc.subject.keywordPlus | BINDING | - |
dc.subject.keywordPlus | PI3K | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
73, Goryeodae-ro, Seongbuk-gu, Seoul, Republic of Korea (02841)82-2-2286-1265
COPYRIGHT 2020 KOREA UNIVERSITY MEDICAL LIBRARY ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.