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MicroRNA-150 regulates the cytotoxicity of natural killers by targeting perforin-1

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dc.contributor.authorKim, Nayoung-
dc.contributor.authorKim, Miju-
dc.contributor.authorYun, Sohyun-
dc.contributor.authorDoh, Junsang-
dc.contributor.authorGreenberg, Philip D.-
dc.contributor.authorKim, Tae-Don-
dc.contributor.authorChoi, Inpyo-
dc.date.accessioned2024-05-20T00:42:13Z-
dc.date.available2024-05-20T00:42:13Z-
dc.date.created2024-05-17-
dc.date.issued2014-07-
dc.identifier.citationJournal of Allergy and Clinical Immunology, Vol.134 No.1, pp.195-+-
dc.identifier.issn0091-6749-
dc.identifier.urihttps://hdl.handle.net/10371/203402-
dc.description.abstractBackground: Perforin-1 (Prf1) is the predominant cytolytic protein secreted by natural killer (NK) cells. For a rapid immune response, resting NK cells contain high Prf1 mRNA concentrations while exhibiting minimal cytotoxicity caused by a blockage of Prf1 protein synthesis, implying that an unknown posttranscriptional regulatory mechanism exists. Objective: We sought to determine whether microRNA-150 (miR-150) posttranscriptionally regulates Prf1 translation in both mouse and human NK cells at rest and at various time points after activation. Methods: Mouse NK cells with a targeted deletion of miR-150 (miR-150(-/-) NK cells), primary human NK cells, and NK92 MI cells were used to investigate the role of miR-150 in NK cells. NK cell cytotoxicity assays and Western blotting proved that activated miR-150(-/-) NK cells expressed upregulated Prf1, augmenting NK cell cytotoxicity. When immunodeficient mice were injected with miR-150(-/-) NK cells, there was a significant reduction in tumor growth and metastasis of B16F10 melanoma. Results: We report that miR-150 binds to 39 untranslated regions of mouse and human Prf1, posttranscriptionally downregulating its expression. Mouse wild-type NK cells displayed downregulated miR-150 expression in response to IL-15, which led to corresponding repression and induction of Prf1 during rest and after IL-15 activation, respectively. Conclusion: Our results indicate that miR-150 is a common posttranscriptional regulator for Prf1 in mouse and human NK cells that represses NK cell lytic activity. Thus the therapeutic control of miR-150 in NK cells could enhance NK cell-based immunotherapy against cancer, providing a better clinical outcome.-
dc.language영어-
dc.publisherMosby Inc.-
dc.titleMicroRNA-150 regulates the cytotoxicity of natural killers by targeting perforin-1-
dc.typeArticle-
dc.identifier.doi10.1016/j.jaci.2014.02.018-
dc.citation.journaltitleJournal of Allergy and Clinical Immunology-
dc.identifier.wosid000338930300025-
dc.identifier.scopusid2-s2.0-84903733656-
dc.citation.endpage+-
dc.citation.number1-
dc.citation.startpage195-
dc.citation.volume134-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorDoh, Junsang-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusNK-CELL CYTOTOXICITY-
dc.subject.keywordPlusGRANZYME-B-
dc.subject.keywordPlusMIR-150-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusLEUKEMIA-
dc.subject.keywordPlusDIFFERENTIATION-
dc.subject.keywordPlusRECOGNITION-
dc.subject.keywordPlusINVOLVEMENT-
dc.subject.keywordPlusRECEPTOR-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordAuthormiR-150-
dc.subject.keywordAuthorNK cells-
dc.subject.keywordAuthorperforin-1-
dc.subject.keywordAuthorNK cell cytotoxicity-
dc.subject.keywordAuthorpost-transcriptional regulation-
dc.subject.keywordAuthorimmunotherapy-
dc.subject.keywordAuthortumor growth and metastasis-
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