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Effect of tobacco compounds on gene expression profiles in human epithelial cells

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dc.contributor.authorSohn, Sung-Hwa-
dc.contributor.authorLee, Jaebum-
dc.contributor.authorKim, Ki-Nam-
dc.contributor.authorKim, In Kyoung-
dc.contributor.authorKim, Meyoung-Kon-
dc.date.accessioned2021-09-08T20:57:12Z-
dc.date.available2021-09-08T20:57:12Z-
dc.date.created2021-06-19-
dc.date.issued2009-01-
dc.identifier.issn1382-6689-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/120778-
dc.description.abstractThis study was carried out to investigate the effects of the tobacco compounds (TC), nicotine, B(a)P, and 2-naphthylamine, on gene expression profiles in a human epithelial cells (A549). We treated A549 with the TC and analyzed gene expression using microarray and real-time PCR (RTP). Gene expression varied according to the TC used. By microarray, we found that apoptosis-related genes such as apoptosis-associated tyrosine kinase, interleukin 10 receptor beta. caspase I and DNA fragmentation factor beta subunit (40 kDa) were down-regulated in TC-treated A549 cells. RTP showed significant increases in the expression of Ahr, Arnt, CYP1A1, and CYP1B1 in TC-treated A549 cells. From these results, we suggest that tobacco compounds can influence apoptosis, inflammation, immunity, and the cell cycle in A549 cells. Also, our study demonstrates that a microarray-based genomic survey is a Suitable high-throughput approach for the evaluation of gene expression and for the characterization of TC-induced toxicity. (C) 2008 Elsevier B.V. All rights reserved.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherELSEVIER-
dc.subjectARYL-HYDROCARBON RECEPTOR-
dc.subjectNUCLEAR TRANSLOCATOR ARNT-
dc.subjectRISK-ASSESSMENT-
dc.subjectAH-RECEPTOR-
dc.subjectCANCER-
dc.subjectCYP1B1-
dc.subjectPROLIFERATION-
dc.subjectACTIVATION-
dc.subjectMECHANISM-
dc.subjectAPOPTOSIS-
dc.titleEffect of tobacco compounds on gene expression profiles in human epithelial cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Meyoung-Kon-
dc.identifier.doi10.1016/j.etap.2008.09.005-
dc.identifier.scopusid2-s2.0-57149145436-
dc.identifier.wosid000262564600016-
dc.identifier.bibliographicCitationENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, v.27, no.1, pp.111 - 119-
dc.relation.isPartOfENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY-
dc.citation.titleENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY-
dc.citation.volume27-
dc.citation.number1-
dc.citation.startPage111-
dc.citation.endPage119-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaEnvironmental Sciences & Ecology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaToxicology-
dc.relation.journalWebOfScienceCategoryEnvironmental Sciences-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryToxicology-
dc.subject.keywordPlusARYL-HYDROCARBON RECEPTOR-
dc.subject.keywordPlusNUCLEAR TRANSLOCATOR ARNT-
dc.subject.keywordPlusRISK-ASSESSMENT-
dc.subject.keywordPlusAH-RECEPTOR-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusCYP1B1-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusMECHANISM-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordAuthorNicotine-
dc.subject.keywordAuthorB(a)P-
dc.subject.keywordAuthor2-Naphthylamine-
dc.subject.keywordAuthorGene expression-
dc.subject.keywordAuthorMicroarray-
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