4.3 Article

miR-125a regulates cell cycle, proliferation, and apoptosis by targeting the ErbB pathway in acute myeloid leukemia

期刊

LEUKEMIA RESEARCH
卷 38, 期 3, 页码 402-410

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.leukres.2013.12.021

关键词

microRNA-125a; Methylation; Cell cycle; Apoptosis; Mubritinib

资金

  1. American Cancer Society Research Grant [IRG-82-003-27]
  2. National Institute of Health National Institute of General Medical Sciences (NIH/NIGMS) COBRE in Stem Cell Biology and Regenerative Medicine [8P20GM103465]
  3. Maine Medical Center Research Institute Core facilities in Genomics and Bioinformatics
  4. Flow Cytometry and Progenitor Cell Analysis
  5. NIH/NIGMS [8P20GM103465]
  6. Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health [8P20GM103449]
  7. [5P30GM103392]

向作者/读者索取更多资源

microRNA profiling of acute myeloid leukemia patient samples identified miR-125a as being decreased. Current literature has investigated miR-125a's role in normal hematopoiesis but not within acute myeloid leukemia. Analysis of the upstream region of miR-125a identified several CpG islands. Both precursor and mature miR-125a increased in response to a de-methylating agent, Decitabine. Profiling revealed the ErbB pathway as significantly decreased with ectopic miR-125a. Either ectopic expression of miR-125a or inhibition of ErbB via Mubritinib resulted in inhibition of cell cycle proliferation and progression with enhanced apoptosis revealing ErbB inhibitors as potential novel therapeutic agents for treating miR-125a-low AML. (C) 2013 Elsevier Ltd. All rights reserved.

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