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A(3) Adenosine Receptor Antagonist, Truncated Thio-Cl-IB-MECA, Induces Apoptosis in T24 Human Bladder Cancer Cells

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dc.contributor.authorKim, Heejong-
dc.contributor.authorKang, Jeong Woo-
dc.contributor.authorLee, Sojung-
dc.contributor.authorChoi, Won Jun-
dc.contributor.authorJeong, Lak Shin-
dc.contributor.authorYang, Young-
dc.contributor.authorHong, Jin Tae-
dc.contributor.authorYoon, Do Young-
dc.date.available2021-02-22T13:47:37Z-
dc.date.created2020-09-03-
dc.date.issued2010-07-
dc.identifier.issn0250-7005-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13179-
dc.description.abstractBackground: Human A(3) adenosine receptor (A(3)AR) plays an essential role in several plzysiopathological processes. Thus far, A(3)AR-selective ligands have been evaluated as anti-inflammation and anticancer therapeutic agents. Among these ligands, truncated thio-Cl-IB-MECA is a newly reported antagonist, and its function has not been studied. Materials and Methods: Cell viability was measured by MTS assay. Cell cycle progression was analysed by propidium iodide (PI) flow cytometric assay. The apoptotic effects were investigated by Hoechst staining and annexin V-FITC/PI staining. The signal-transduction mechanism was explored by Western blot. Results: Truncated thio-Cl-IB-MECA induced the growth arrest of T24 cells at sub-G(1) phase and provoked apoptosis but not necrosis. Apoptotic death was mediated by the activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). Conclusion: Since truncated thio-Cl-IB-MECA induces anti-proliferation and apoptotic effects via ERK and JNK activation, it may function as an anticancer agent in human bladder cancer cells.-
dc.language영어-
dc.language.isoen-
dc.publisherINT INST ANTICANCER RESEARCH-
dc.titleA(3) Adenosine Receptor Antagonist, Truncated Thio-Cl-IB-MECA, Induces Apoptosis in T24 Human Bladder Cancer Cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorYang, Young-
dc.identifier.scopusid2-s2.0-77955819668-
dc.identifier.wosid000280796400047-
dc.identifier.bibliographicCitationANTICANCER RESEARCH, v.30, no.7, pp.2823 - 2830-
dc.relation.isPartOfANTICANCER RESEARCH-
dc.citation.titleANTICANCER RESEARCH-
dc.citation.volume30-
dc.citation.number7-
dc.citation.startPage2823-
dc.citation.endPage2830-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusTUMOR-GROWTH INHIBITION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusAGONISTS-
dc.subject.keywordPlusDEATH-
dc.subject.keywordPlusHL-60-
dc.subject.keywordPlusERK-
dc.subject.keywordPlusD-4&apos-
dc.subject.keywordPlus-THIOADENOSINE-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusDERIVATIVES-
dc.subject.keywordPlusTHERAPY-
dc.subject.keywordAuthorA3 adenosine receptor-
dc.subject.keywordAuthorA3AR antagonist-
dc.subject.keywordAuthorApoptosis-
dc.subject.keywordAuthorTruncated thio-Cl-IB-MECA-
dc.identifier.urlhttps://ar.iiarjournals.org/content/30/7/2823.short-
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