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Potentiation of etoposide-induced apoptosis in HeLa cells by co-treatment with KG-135, a quality-controlled standardized ginsenoside formulation
DC Field | Value | Language |
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dc.contributor.author | Lee, Won-Hee | - |
dc.contributor.author | Choi, Joon-Seok | - |
dc.contributor.author | Kim, Hyun Young | - |
dc.contributor.author | Park, Jeong-Hill | - |
dc.contributor.author | Park, Byoung Duck | - |
dc.contributor.author | Cho, Seung Ju | - |
dc.contributor.author | Lee, Seung-Ki | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2021-01-31T09:23:51Z | - |
dc.date.available | 2021-01-31T09:23:51Z | - |
dc.date.created | 2017-11-15 | - |
dc.date.issued | 2010-08 | - |
dc.identifier.citation | Cancer Letters, Vol.294 No.1, pp.74-81 | - |
dc.identifier.issn | 0304-3835 | - |
dc.identifier.other | 2541 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172638 | - |
dc.description.abstract | Our previous studies demonstrated that KG-135, a quality-controlled red ginseng-specific formulation containing approximately equal amounts of three major ginsenosides (Rk1, Rg3 and Rg5), down-regulated Cl cyclin-dependent kinase in HeLa cells. In the present work, we have found that KG-135 potentates cytotoxicity of etoposide by modulating apoptotic signaling. Co-treatment of etoposide and KG-135 markedly elevated the expression and phosphorylation at the serine 15 residue of p53 as well as the cellular levels of Bax and p21(Waf1/Cip1). The increased accumulation and phosphorylation of p53 (Ser15) were attenuated by treatment of cells with wortmannin, a pan-phosphatidylinosito1-3 kinase inhibitor. Moreover, co-treatment of etoposide and KG-135 enhanced mitochondrial localization of Bax. Our results indicate that etoposide-induced apoptosis in HeLa cells can be potentiated in the presence of KG-135 through a mechanism that involves the stabilization of p53 and the stimulation of Bax- and p21-mediated apoptotic signaling pathways. These findings suggest that KG-135 represents a useful candidate adjuvant for the treatment of cancers that could potentially minimize the adverse effects of current clinical chemotherapeutics. (C) 2010 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | 영어 | - |
dc.publisher | Elsevier BV | - |
dc.title | Potentiation of etoposide-induced apoptosis in HeLa cells by co-treatment with KG-135, a quality-controlled standardized ginsenoside formulation | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 서영준 | - |
dc.identifier.doi | 10.1016/j.canlet.2010.01.024 | - |
dc.citation.journaltitle | Cancer Letters | - |
dc.identifier.wosid | 000278799100009 | - |
dc.identifier.scopusid | 2-s2.0-77953027035 | - |
dc.citation.endpage | 81 | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 74 | - |
dc.citation.volume | 294 | - |
dc.identifier.sci | 000278799100009 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Park, Jeong-Hill | - |
dc.contributor.affiliatedAuthor | Lee, Seung-Ki | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | DAMAGE-INDUCED PHOSPHORYLATION | - |
dc.subject.keywordPlus | ELEVATES PROTEIN-LEVELS | - |
dc.subject.keywordPlus | SK-HEP-1 CELLS | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | POSTTRANSLATIONAL MODIFICATIONS | - |
dc.subject.keywordPlus | CANCER CELLS | - |
dc.subject.keywordPlus | P53 | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | ATM | - |
dc.subject.keywordPlus | P21(WAF1) | - |
dc.subject.keywordAuthor | Etoposide | - |
dc.subject.keywordAuthor | Ginseng | - |
dc.subject.keywordAuthor | KG-135 | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordAuthor | p53 | - |
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