BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023736%3A_____%2F18%3A00012154" target="_blank" >RIV/00023736:_____/18:00012154 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11110/18:10385555
Result on the web
<a href="https://doi.org/10.3324/haematol.2018.193086" target="_blank" >https://doi.org/10.3324/haematol.2018.193086</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3324/haematol.2018.193086" target="_blank" >10.3324/haematol.2018.193086</a>
Alternative languages
Result language
angličtina
Original language name
BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia
Original language description
The fusion oncoprotein BCR-ABL1 exhibits aberrant tyrosine kinase activity and has been proposed to deregulate signaling networks involving both transcription factors and non-coding microRNAs that result in chronic myeloid leukemia. Previously, microRNA expression profiling showed deregulated expression of miR-150 and miR-155 in chronic myeloid leukemia. In this study, we placed these findings into the broader context of the MYC/miR-150/MYB/miR-155/PU.1 oncogenic network. We propose that upregulated MYC and miR-155 in CD34+ leukemic stem and progenitor cells in concert with BCR-ABL1 impair the molecular mechanisms of myeloid differentiation associated with low miR-150 and PU.1 levels. We revealed that MYC directly occupied the -11.7 kb and -0.35 kb regulatory regions in the MIR150 gene. MYC occupancy was markedly increased through BCR-ABL1 activity, causing inhibition of MIR150 gene expression in chronic myeloid leukemia CD34+ and CD34- cells
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30205 - Hematology
Result continuities
Project
<a href="/en/project/LH15104" target="_blank" >LH15104: Study of the epigenetic factors and tumor-suppressor genes regulating oncogene signaling pathways in models of leukemic hematopoiesis</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Haematologica
ISSN
0390-6078
e-ISSN
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Volume of the periodical
103
Issue of the periodical within the volume
12
Country of publishing house
IT - ITALY
Number of pages
10
Pages from-to
2016-2025
UT code for WoS article
000451736600026
EID of the result in the Scopus database
2-s2.0-85060844821