Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Su-Hwa | - |
dc.contributor.author | Park, Eun-Jung | - |
dc.contributor.author | Lee, Chae Ryun | - |
dc.contributor.author | Chun, Jung Nyeo | - |
dc.contributor.author | Cho, Nam-Hyuk | - |
dc.contributor.author | Kim, In-Gyu | - |
dc.contributor.author | Lee, Sanghoon | - |
dc.contributor.author | Kim, Tae Woo | - |
dc.contributor.author | Park, Hyun Ho | - |
dc.contributor.author | So, Insuk | - |
dc.contributor.author | Jeon, Ju-Hong | - |
dc.date.accessioned | 2021-09-06T20:19:32Z | - |
dc.date.available | 2021-09-06T20:19:32Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2012-05 | - |
dc.identifier.issn | 1019-6439 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/108525 | - |
dc.description.abstract | Geraniol, an acyclic dietary monoterpene, suppresses prostate cancer growth and enhances docetaxel chemosensitivity in cultured cell or xenograft tumor models. However, the mechanisms of the geraniol action against prostate cancer are largely unknown. In this study, we investigated the cellular and molecular mechanisms of geraniol-induced cell death in PC-3 prostate cancer cells. Among the examined structurally and functionally similar monoterpenes, geraniol potently induced apoptosis and autophagy. Although independent processes, apoptosis and autophagy acted as cooperative partners to elicit geraniol-induced cell death in PC-3 cells. At a molecular level, geraniol inhibited Ala signaling and activated AMPK signaling, resulting in mTOR inhibition. Combined treatment of AKT inhibitor and AMPK activator markedly suppressed cell growth compared to either treatment alone. Our findings provide insight into future investigations that are aimed at elucidating the role of apoptosis and autophagy in prostate cancer therapy and at developing anticancer strategies co-targeting AKT and AMPK. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | SPANDIDOS PUBL LTD | - |
dc.subject | PTEN | - |
dc.subject | GROWTH | - |
dc.subject | BIOSYNTHESIS | - |
dc.subject | INACTIVATION | - |
dc.subject | RESISTANCE | - |
dc.subject | FARNESOL | - |
dc.subject | TARGET | - |
dc.title | Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Tae Woo | - |
dc.identifier.doi | 10.3892/ijo.2011.1318 | - |
dc.identifier.scopusid | 2-s2.0-84860312860 | - |
dc.identifier.wosid | 000302273400042 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF ONCOLOGY, v.40, no.5, pp.1683 - 1690 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF ONCOLOGY | - |
dc.citation.title | INTERNATIONAL JOURNAL OF ONCOLOGY | - |
dc.citation.volume | 40 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 1683 | - |
dc.citation.endPage | 1690 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | PTEN | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | BIOSYNTHESIS | - |
dc.subject.keywordPlus | INACTIVATION | - |
dc.subject.keywordPlus | RESISTANCE | - |
dc.subject.keywordPlus | FARNESOL | - |
dc.subject.keywordPlus | TARGET | - |
dc.subject.keywordAuthor | geraniol | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordAuthor | cell death | - |
dc.subject.keywordAuthor | prostate cancer | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. 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.