Arctigenin shows preferential cytotoxicity to acidity-tolerant prostate carcinoma PC-3 cells through ROS-mediated mitochondrial damage and the inhibition of PI3K/Akt/mTOR pathway
DC Field | Value | Language |
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dc.contributor.author | Lee, Yoon-Jin | - |
dc.contributor.author | Oh, Jeong-Eun | - |
dc.contributor.author | Lee, Sang-Han | - |
dc.date.accessioned | 2021-08-11T11:24:07Z | - |
dc.date.available | 2021-08-11T11:24:07Z | - |
dc.date.issued | 2018-11-10 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5498 | - |
dc.description.abstract | Extracellular acidity in the tumor microenvironment contributes to chemoresistance of malignant tumors. The objective of this study was to determine anticancer effects of arctigenin, a novel anti-inflammatory lignan extracted from seeds of Arctium lappa, on acidity-tolerant prostate cancer PC-3AcT cells. The PC-3AcT cells manifested increased tolerance to low-pH media with enhanced percent cell viability and increased resistance to docetaxel compared to their parental PC-3 cells. Arctigenin alone or in combination with docetaxel induced potent cytotoxicity. Preferential sensitization of PC-3AcT cells to arctigenin was accompanied by increased cell fractions with sub-G(0)/G(1) peak and annexin V-PE(+), increased ROS levels, decreased mitochondrial membrane potential and cellular ATP content, and inhibition of PI3K/Akt/mTOR pathway. A series of changes caused by arctigenin were efficiently reversed through reducing ROS levels by radical scavenger N-acetylcysteine, thus placing ROS upstream of arctigenin-driven cytotoxicity. Collectively, these results demonstrate that arctigenin can increase oxidative stress-mediated mitochondrial damage of acidity-tolerant PC-3AcT cells, suggesting that arctigenin might be a potential therapeutic candidate to overcome acidic-microenvironment-associated chemotherapeutic resistance in prostate cancer. (C) 2018 Elsevier Inc. All rights reserved. | - |
dc.format.extent | 7 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Academic Press | - |
dc.title | Arctigenin shows preferential cytotoxicity to acidity-tolerant prostate carcinoma PC-3 cells through ROS-mediated mitochondrial damage and the inhibition of PI3K/Akt/mTOR pathway | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1016/j.bbrc.2018.10.045 | - |
dc.identifier.scopusid | 2-s2.0-85054714810 | - |
dc.identifier.wosid | 000450019400045 | - |
dc.identifier.bibliographicCitation | Biochemical and Biophysical Research Communications, v.505, no.4, pp 1244 - 1250 | - |
dc.citation.title | Biochemical and Biophysical Research Communications | - |
dc.citation.volume | 505 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 1244 | - |
dc.citation.endPage | 1250 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.subject.keywordPlus | ACTIVATED PROTEIN-KINASE | - |
dc.subject.keywordPlus | CANCER-CELLS | - |
dc.subject.keywordPlus | COMPLEX-I | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordAuthor | Arctigenin | - |
dc.subject.keywordAuthor | Prostate cancer | - |
dc.subject.keywordAuthor | Chemoresistance | - |
dc.subject.keywordAuthor | Reactive oxygen species | - |
dc.subject.keywordAuthor | Extracellular acidity | - |
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