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MicroRNA-150 regulates the cytotoxicity of natural killers by targeting perforin-1
DC Field | Value | Language |
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dc.contributor.author | Kim, Nayoung | - |
dc.contributor.author | Kim, Miju | - |
dc.contributor.author | Yun, Sohyun | - |
dc.contributor.author | Doh, Junsang | - |
dc.contributor.author | Greenberg, Philip D. | - |
dc.contributor.author | Kim, Tae-Don | - |
dc.contributor.author | Choi, Inpyo | - |
dc.date.accessioned | 2024-05-20T00:42:13Z | - |
dc.date.available | 2024-05-20T00:42:13Z | - |
dc.date.created | 2024-05-17 | - |
dc.date.issued | 2014-07 | - |
dc.identifier.citation | Journal of Allergy and Clinical Immunology, Vol.134 No.1, pp.195-+ | - |
dc.identifier.issn | 0091-6749 | - |
dc.identifier.uri | https://hdl.handle.net/10371/203402 | - |
dc.description.abstract | Background: 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.language | 영어 | - |
dc.publisher | Mosby Inc. | - |
dc.title | MicroRNA-150 regulates the cytotoxicity of natural killers by targeting perforin-1 | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.jaci.2014.02.018 | - |
dc.citation.journaltitle | Journal of Allergy and Clinical Immunology | - |
dc.identifier.wosid | 000338930300025 | - |
dc.identifier.scopusid | 2-s2.0-84903733656 | - |
dc.citation.endpage | + | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 195 | - |
dc.citation.volume | 134 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Doh, Junsang | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | NK-CELL CYTOTOXICITY | - |
dc.subject.keywordPlus | GRANZYME-B | - |
dc.subject.keywordPlus | MIR-150 | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | LEUKEMIA | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | RECOGNITION | - |
dc.subject.keywordPlus | INVOLVEMENT | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordAuthor | miR-150 | - |
dc.subject.keywordAuthor | NK cells | - |
dc.subject.keywordAuthor | perforin-1 | - |
dc.subject.keywordAuthor | NK cell cytotoxicity | - |
dc.subject.keywordAuthor | post-transcriptional regulation | - |
dc.subject.keywordAuthor | immunotherapy | - |
dc.subject.keywordAuthor | tumor growth and metastasis | - |
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