Alleviation of the drug-resistant phenotype in idarubicin and cytosine arabinoside double-resistant acute myeloid leukemia cells by indomethacin
DC Field | Value | Language |
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dc.contributor.author | Song, Ju Han | - |
dc.contributor.author | Kim, Seung Hyun | - |
dc.contributor.author | Kim, Hyeoung-Joon | - |
dc.contributor.author | Hwang, Seung Yong | - |
dc.contributor.author | Kim, Tae Sung | - |
dc.date.accessioned | 2021-09-09T09:42:13Z | - |
dc.date.available | 2021-09-09T09:42:13Z | - |
dc.date.created | 2021-06-10 | - |
dc.date.issued | 2008-04 | - |
dc.identifier.issn | 1019-6439 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/123806 | - |
dc.description.abstract | Chemoresistance to anticancer drugs is a major issue in the successful treatment of acute myeloid leukemia (AML). In this study, we developed an AML cell line (AML-2/IDAC) that is resistant to treatment with a combination of idarubicin and cytosine arabinoside (Id/AraC) by chronic exposure for more than 3 months. We then investigated the ability of indomethacin to alleviate the chemoresistance of AML-2/IDAC cells. Treatment with indomethacin alone induced growth arrest, but not the death of AML-2/IDAC cells. However, when AML-2/IDAC cells were treated with combinations of indomethacin and Id/AraC, the cell death and apoptosis rate of AML-2/IDAC cells were significantly increased in a dose- and time-dependent manner. The combined treatment with indomethacin and Id/AraC caused the collapse of the mitochondrial membrane potential and was also demonstrated to enhance the activities of caspase-3 and -8 in AML-2/IDAC cells. Furthermore, indomethacin down-regulated expression of the ABCA3 and MRP1 genes, which were over-expressed in AML-2/IDAC cells. Taken together, the results of this study suggest that indomethacin can be used to increase the therapeutic potential against drug-resistant AML when combined with anti-leukemic drugs. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | PROFESSOR D A SPANDIDOS | - |
dc.subject | ACUTE LYMPHOBLASTIC-LEUKEMIA | - |
dc.subject | CHRONIC LYMPHOCYTIC-LEUKEMIA | - |
dc.subject | INHIBITS PROLIFERATION | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | T-CELLS | - |
dc.subject | IN-VIVO | - |
dc.subject | APOPTOSIS | - |
dc.subject | THERAPY | - |
dc.subject | ABCA3 | - |
dc.subject | DAUNORUBICIN | - |
dc.title | Alleviation of the drug-resistant phenotype in idarubicin and cytosine arabinoside double-resistant acute myeloid leukemia cells by indomethacin | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Tae Sung | - |
dc.identifier.scopusid | 2-s2.0-44449120041 | - |
dc.identifier.wosid | 000254357600022 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF ONCOLOGY, v.32, no.4, pp.931 - 936 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF ONCOLOGY | - |
dc.citation.title | INTERNATIONAL JOURNAL OF ONCOLOGY | - |
dc.citation.volume | 32 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 931 | - |
dc.citation.endPage | 936 | - |
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 | ACUTE LYMPHOBLASTIC-LEUKEMIA | - |
dc.subject.keywordPlus | CHRONIC LYMPHOCYTIC-LEUKEMIA | - |
dc.subject.keywordPlus | INHIBITS PROLIFERATION | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | T-CELLS | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | THERAPY | - |
dc.subject.keywordPlus | ABCA3 | - |
dc.subject.keywordPlus | DAUNORUBICIN | - |
dc.subject.keywordAuthor | ABC-transporter | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | drug-resistance | - |
dc.subject.keywordAuthor | indomethacin | - |
dc.subject.keywordAuthor | acute myeloid leukemia | - |
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