ArticleBlood cancer journal2013
MR-1 blocks the megakaryocytic differentiation and transition of CML from chronic phase to blast crisis through MEK dephosphorylation.
Article in Blood cancer journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- DYT8 drives lung adenocarcinoma through EGFR-mediated PSMC6 recruitment and uncharacterized phosphorylation at Ser 306 and 525 of c-Src.Acta pharmacologica Sinica · 2026Article
- Establishment of a novel mesenchymal stem cell-based regimen for chronic myeloid leukemia differentiation therapy.Cell death & disease · 2021Article
- Cyclizing-berberine A35 induces G2/M arrest and apoptosis by activating YAP phosphorylation (Ser127).Journal of experimental & clinical cancer research : CR · 2018Article
- Sophoridinol derivative 05D induces tumor cells apoptosis by topoisomerase1-mediated DNA breakage.OncoTargets and therapy · 2016Article
- Article
- Genetic events other than BCR-ABL1.Current hematologic malignancy reports · 2014Review
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Authors and funding
7 authors.
Funding
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Abstract
Chronic myelogenous leukemia (CML) evolves from a chronic phase characterized by the Philadelphia chromosome as the sole genetic abnormality and the accumulation of mature cells in peripheral blood into blast crisis, which is characterized by the rapid expansion of myeloid- or lymphoid-differentiation-arrested blast cells. Although ample studies have been conducted on the disease progress mechanisms, the underlying molecular mechanisms of the malignant phenotype transition are still unclear. In this study, we have shown that myofibrillogenesis regulator-1 (MR-1) was overexpressed in blast crisis patients and leukemic cells, but there was little trace expressed in healthy individuals and in most patients in CML chronic phase. MR-1 could inhibit the differentiation of myeloid cells into megakaryocytic lineages and accelerate cell proliferation. The molecular mechanism responsible for these effects was the interaction of MR-1 with MEK, which blocked the MEK/ERK signaling pathway by dephosphorylating MEK. Our results provide compelling and important evidence that MR-1 might act as a diagnostic marker and potential target of CML progression from chronic phase to blast crisis.
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Registered trials
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