Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells
Identifieur interne : 003043 ( Main/Merge ); précédent : 003042; suivant : 003044Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells
Auteurs : Susumu Goyama [États-Unis] ; Janet Schibler [États-Unis] ; Lea Cunningham [États-Unis] ; Yue Zhang [États-Unis] ; Yalan Rao [États-Unis] ; Nahoko Nishimoto [Japon] ; Masahiro Nakagawa [Japon] ; Andre Olsson [États-Unis] ; Mark Wunderlich [États-Unis] ; Kevin A. Link [États-Unis] ; Benjamin Mizukawa [États-Unis] ; H. Leighton Grimes [États-Unis] ; Mineo Kurokawa [Japon] ; P. Paul Liu [États-Unis] ; Gang Huang [États-Unis] ; James C. Mulloy [États-Unis]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; 2013.
Abstract
RUNX1 is generally considered a tumor suppressor in myeloid neoplasms. Inactivating RUNX1 mutations have frequently been found in patients with myelodysplastic syndrome (MDS) and cytogenetically normal acute myeloid leukemia (AML). However, no somatic RUNX1 alteration was found in AMLs with leukemogenic fusion proteins, such as core-binding factor (CBF) leukemia and MLL fusion leukemia, raising the possibility that RUNX1 could actually promote the growth of these leukemia cells. Using normal human cord blood cells and those expressing leukemogenic fusion proteins, we discovered a dual role of RUNX1 in myeloid leukemogenesis. RUNX1 overexpression inhibited the growth of normal cord blood cells by inducing myeloid differentiation, whereas a certain level of RUNX1 activity was required for the growth of AML1-ETO and MLL-AF9 cells. Using a mouse genetic model, we also showed that the combined loss of
Url:
DOI: 10.1172/JCI68557
PubMed: 23979164
PubMed Central: 3754260
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<author><name sortKey="Huang, Gang" sort="Huang, Gang" uniqKey="Huang G" first="Gang" last="Huang">Gang Huang</name>
<affiliation wicri:level="2"><nlm:aff id="JCI68557">Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Mulloy, James C" sort="Mulloy, James C" uniqKey="Mulloy J" first="James C." last="Mulloy">James C. Mulloy</name>
<affiliation wicri:level="2"><nlm:aff id="JCI68557">Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea>
<placeName><region type="state">Ohio</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">The Journal of Clinical Investigation</title>
<idno type="ISSN">0021-9738</idno>
<idno type="eISSN">1558-8238</idno>
<imprint><date when="2013">2013</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>RUNX1 is generally considered a tumor suppressor in myeloid neoplasms. Inactivating RUNX1 mutations have frequently been found in patients with myelodysplastic syndrome (MDS) and cytogenetically normal acute myeloid leukemia (AML). However, no somatic RUNX1 alteration was found in AMLs with leukemogenic fusion proteins, such as core-binding factor (CBF) leukemia and MLL fusion leukemia, raising the possibility that RUNX1 could actually promote the growth of these leukemia cells. Using normal human cord blood cells and those expressing leukemogenic fusion proteins, we discovered a dual role of RUNX1 in myeloid leukemogenesis. RUNX1 overexpression inhibited the growth of normal cord blood cells by inducing myeloid differentiation, whereas a certain level of RUNX1 activity was required for the growth of AML1-ETO and MLL-AF9 cells. Using a mouse genetic model, we also showed that the combined loss of <italic>Runx1/Cbfb</italic>
inhibited leukemia development induced by MLL-AF9. RUNX2 could compensate for the loss of RUNX1. The survival effect of RUNX1 was mediated by BCL2 in MLL fusion leukemia. Our study unveiled an unexpected prosurvival role for RUNX1 in myeloid leukemogenesis. Inhibiting RUNX1 activity rather than enhancing it could be a promising therapeutic strategy for AMLs with leukemogenic fusion proteins.
</p>
</div>
</front>
</TEI>
</record>
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