Selective cell death of oncogenic Akt-transduced brain cancer cells by etoposide through reactive oxygen species-mediated damage
DC Field | Value | Language |
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dc.contributor.author | Oh, Se-Yeong | - |
dc.contributor.author | Sohn, Young-Woo | - |
dc.contributor.author | Park, Jong-Whi | - |
dc.contributor.author | Park, Hyo-Jung | - |
dc.contributor.author | Jeon, Hye-Min | - |
dc.contributor.author | Kim, Tae-Kyung | - |
dc.contributor.author | Lee, Joong-Seob | - |
dc.contributor.author | Jung, Ji-Eun | - |
dc.contributor.author | Jin, Xun | - |
dc.contributor.author | Chung, Yong Gu | - |
dc.contributor.author | Choi, Young-Ki | - |
dc.contributor.author | You, Seungkwon | - |
dc.contributor.author | Lee, Jang-Bo | - |
dc.contributor.author | Kim, Hyunggee | - |
dc.date.accessioned | 2022-02-28T07:40:40Z | - |
dc.date.available | 2022-02-28T07:40:40Z | - |
dc.date.created | 2022-02-28 | - |
dc.date.issued | 2007-08 | - |
dc.identifier.issn | 1535-7163 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/83593 | - |
dc.description.abstract | We have established several glioma-relevant oncogene-engineered cancer cells to reevaluate the oncogene-selective cytotoxicity of previously well-characterized anticancer drugs, such as etoposide, doxorubicin, staurosporine, and carmustine. Among several glioma-relevant oncogenes (activated epidermal growth factor receptor, Ras, and Akt, as well as Bcl-2 and p53DD used in the present study), the activated epidermal growth factor receptor, Ras, and Akt exerted oncogenic transformation of Ink4a/Arf(-/-) murine astrocyte cells. We identified that etoposide, a topoisomerase 11 inhibitor, caused selective killing of myristylated Akt (Akt-myr) - transduced Ink4a/Arf(-/-) astrocytes and U87MG cells in a dose- and time-dependent manner. Etoposide-selective cytotoxicity in the Akt-myr - transduced cells was shown to be caused by nonapoptotic cell death and occurred in a p53-independent manner. Etoposide caused severe reactive oxygen species (ROS) accumulation preferentially in the Akt-myr-transduced cells, and elevated ROS rendered these cells highly sensitive to cell death. The etoposideselective cell death of Akt-myr-transduced cells was attenuated by pepstatin A, a lysosomal protease inhibitor. In the present study, we show that etoposide might possess a novel therapeutic activity for oncogenic Akt-transduced cancer cells to kill preferentially through ROS-mediated-damage. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | AMER ASSOC CANCER RESEARCH | - |
dc.relation.isPartOf | MOLECULAR CANCER THERAPEUTICS | - |
dc.title | Selective cell death of oncogenic Akt-transduced brain cancer cells by etoposide through reactive oxygen species-mediated damage | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000248663000005 | - |
dc.identifier.doi | 10.1158/1535-7163.MCT-07-0111 | - |
dc.identifier.bibliographicCitation | MOLECULAR CANCER THERAPEUTICS, v.6, no.8, pp.2178 - 2187 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-34548101114 | - |
dc.citation.endPage | 2187 | - |
dc.citation.startPage | 2178 | - |
dc.citation.title | MOLECULAR CANCER THERAPEUTICS | - |
dc.citation.volume | 6 | - |
dc.citation.number | 8 | - |
dc.contributor.affiliatedAuthor | Park, Jong-Whi | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR | - |
dc.subject.keywordPlus | FIBROBLASTS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | AUTOPHAGY | - |
dc.subject.keywordPlus | MODULATOR | - |
dc.subject.keywordPlus | NECROSIS | - |
dc.subject.keywordPlus | FREQUENT | - |
dc.subject.keywordPlus | GLIOMA | - |
dc.subject.keywordPlus | GENES | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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