Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 최준호 | - |
dc.date.accessioned | 2020-08-14T06:36:25Z | - |
dc.date.available | 2020-08-14T06:36:25Z | - |
dc.date.issued | 2019-07 | - |
dc.identifier.citation | CELL STEM CELL, v. 25, no. 1, Page. 137-148 | en_US |
dc.identifier.issn | 1934-5909 | - |
dc.identifier.issn | 1875-9777 | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S1934590919301201?via%3Dihub | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/152292 | - |
dc.description.abstract | Acute myeloid leukemia (AML) is an aggressive clonal disorder of hematopoietic stem cells (HSCs) and primitive progenitors that blocks their myeloid differentiation, generating self-renewing leukemic stem cells (LSCs). Here, we show that the mRNA m(6)A reader YTHDF2 is overexpressed in a broad spectrum of humanAML and is required for disease initiation as well as propagation in mouse and human AML. YTHDF2 decreases the half-life of diverse m(6)A transcripts that contribute to the overall integrity of LSC function, including the tumor necrosis factor receptor Tnfrsf2, whose upregulation in Ythdf2-deficient LSCs primes cells for apoptosis. Intriguingly, YTHDF2 is not essential for normal HSC function, with YTHDF2 deficiency actually enhancing HSC activity. Thus, we identify YTHDF2 as a unique therapeutic target whose inhibition selectively targets LSCs while promoting HSC expansion. | en_US |
dc.description.sponsorship | K.R.K. is a Cancer Research UK (CRUK) Senior Cancer Research Fellow and a CRUK Programme Grant holder. This work is funded by CRUK (awards C29967/A14633 and C29967/A26787 to K.R.K.) and Wellcome (award 106144 to D.O.). K.R.K.'s laboratory is also supported by grants from The Barts Charity, Wellcome, Bloodwise, Medical Research Council, and the Kay Kendall Leukaemia Fund. D. O. is a member of the Wellcome Centre for Cell Biology supported by Wellcome core funding (award 092076). G.J.S. and T.C.P.S. are supported by CRUK (award C5759/A20971). Part of this work was carried out in the framework of the European Cost Action EPITRAN CA16120. We thank Vladimir Benes and Jelena Pistolic (Genomics Core facility, European Molecular Biology Laboratory, Heidelberg) for performing the gene expression profiling. Brian Huntly and Eric So kindly provided MOZTIF2 and PML-RARA plasmids, respectively. | en_US |
dc.language.iso | en | en_US |
dc.publisher | CELL PRESS | en_US |
dc.subject | MESSENGER-RNA | en_US |
dc.subject | NUCLEAR-RNA | en_US |
dc.subject | EXPRESSION | en_US |
dc.subject | TRANSLATION | en_US |
dc.subject | DIFFERENTIATION | en_US |
dc.subject | HIF-1-ALPHA | en_US |
dc.subject | GENES | en_US |
dc.subject | N6-METHYLADENOSINE | en_US |
dc.subject | LEUKEMOGENESIS | en_US |
dc.subject | IDENTIFICATION | en_US |
dc.title | Targeting the RNA m(6)A Reader YTHDF2 Selectively Compromises Cancer Stem Cells in Acute Myeloid Leukemia | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 25 | - |
dc.identifier.doi | 10.1016/j.stem.2019.03.021 | - |
dc.relation.page | 137-137 | - |
dc.relation.journal | CELL STEM CELL | - |
dc.contributor.googleauthor | Paris, Jasmin | - |
dc.contributor.googleauthor | Morgan, Marcos | - |
dc.contributor.googleauthor | Campos, Joana | - |
dc.contributor.googleauthor | Spencer, Gary J. | - |
dc.contributor.googleauthor | Shmakova, Alena | - |
dc.contributor.googleauthor | Ivanova, Ivayla | - |
dc.contributor.googleauthor | Mapperley, Christopher | - |
dc.contributor.googleauthor | Lawson, Hannah | - |
dc.contributor.googleauthor | Wotherspoon, David A. | - |
dc.contributor.googleauthor | Choe, Junho | - |
dc.relation.code | 2019000197 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF NATURAL SCIENCES[S] | - |
dc.sector.department | DEPARTMENT OF LIFE SCIENCE | - |
dc.identifier.pid | jcho2711 | - |
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