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dc.contributor.authorKim, Hanna-
dc.contributor.authorKim, Su-Nam-
dc.contributor.authorPark, Yeon-Suk-
dc.contributor.authorKim, Nam Hyun-
dc.contributor.authorHan, Jeung Whan-
dc.contributor.authorLee, Hoi Young-
dc.contributor.authorKim, Yong Kee-
dc.date.accessioned2024-01-20T17:32:36Z-
dc.date.available2024-01-20T17:32:36Z-
dc.date.created2021-09-02-
dc.date.issued2011-03-
dc.identifier.issn1019-6439-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/130602-
dc.description.abstractAlthough histone deacetylase (HDAC) inhibitors are emerging as a promising class of cancer chemotherapeutic agents, their effects on multidrug resistance (MDR) are poorly understood. In this study, we investigated whether HDAC inhibitors overcome MDR phenotype. HDAC inhibitors suppress the growth of both MDR positive cancer cells KBV20C and its parental cells KB with similar potencies. In parallel, histone acetylation and p21(WAF1) expression by the HDAC inhibitors were similarly increased in both cell types, indicating that these HDAC inhibitors are poor substrates of ABC drug transporters and effective in MDR cancer cells. In addition, multidrug resistance protein 2 (MRP2) expression is selectively attenuated by HDAC inhibitors, especially SAHA and TSA, in KBV20C cells, whereas MDR1 and BCRP expressions are not affected. This downregulation of MRP2 contributes to increase in paclitaxel-induced G(2)/M arrest and apoptosis, which might be due to intracellular accumulation of paclitaxel. Collectively, our data provide a molecular rationale for the application of HDAC inhibitors to overcome MDR in cancer cells.-
dc.languageEnglish-
dc.publisherSPANDIDOS PUBL LTD-
dc.subjectHISTONE DEACETYLASE INHIBITOR-
dc.subjectSUBEROYLANILIDE HYDROXAMIC ACID-
dc.subjectPROMYELOCYTIC LEUKEMIA-CELLS-
dc.subjectP-GLYCOPROTEIN-
dc.subjectPHASE-I-
dc.subjectDEPSIPEPTIDE FR901228-
dc.subjectDRUG-RESISTANCE-
dc.subjectPROMOTER REGION-
dc.subjectAPICIDIN-
dc.subjectINDUCTION-
dc.titleHDAC inhibitors downregulate MRP2 expression in multidrug resistant cancer cells: Implication for chemosensitization-
dc.typeArticle-
dc.identifier.doi10.3892/ijo.2010.879-
dc.description.journalClass1-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF ONCOLOGY, v.38, no.3, pp.807 - 812-
dc.citation.titleINTERNATIONAL JOURNAL OF ONCOLOGY-
dc.citation.volume38-
dc.citation.number3-
dc.citation.startPage807-
dc.citation.endPage812-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000287829200023-
dc.identifier.scopusid2-s2.0-79952029403-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalResearchAreaOncology-
dc.type.docTypeArticle-
dc.subject.keywordPlusHISTONE DEACETYLASE INHIBITOR-
dc.subject.keywordPlusSUBEROYLANILIDE HYDROXAMIC ACID-
dc.subject.keywordPlusPROMYELOCYTIC LEUKEMIA-CELLS-
dc.subject.keywordPlusP-GLYCOPROTEIN-
dc.subject.keywordPlusPHASE-I-
dc.subject.keywordPlusDEPSIPEPTIDE FR901228-
dc.subject.keywordPlusDRUG-RESISTANCE-
dc.subject.keywordPlusPROMOTER REGION-
dc.subject.keywordPlusAPICIDIN-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordAuthorHDAC inhibitor-
dc.subject.keywordAuthormultidrug resistance-
dc.subject.keywordAuthorMRP2-
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