miRNAs in chronic myeloid leukemia: small molecules, essential function

Leuk Lymphoma. 2017 Jun;58(6):1297-1305. doi: 10.1080/10428194.2016.1243676. Epub 2016 Oct 13.

Abstract

Chronic myeloid leukemia (CML) is a myeloproliferative disorder associated with clonal expansion of cancerous bone marrow stem cells. Tyrosine kinase inhibitors (TKIs) targeting Bcr-Abl oncoprotein are the first-line therapy for most CML patients, however, some are unresponsive to it or develop resistance. Recently, microRNAs (miRNAs) have been implicated in the progression of CML and the development of TKI resistance based on their important regulatory function in cell homeostasis. MicroRNAs are small noncoding RNAs that post-transcriptionally regulate gene expression. Since microRNAs can function either as oncogenes or tumor suppressor genes in leukemogenesis, the potential of using them as therapeutic targets by inhibiting or amplifying their activity, opens up new opportunities for leukemia therapy. In this review, we focus on recent studies on the important roles of microRNAs in the pathogenesis of CML and their relevance as biomarkers for diagnosis, monitoring disease progression, and treatment response.

Keywords: BCR-ABL; CML; MicroRNA; chronic myeloid leukemia.

Publication types

  • Review

MeSH terms

  • Animals
  • Drug Resistance, Neoplasm / genetics
  • Epigenesis, Genetic / drug effects
  • Fusion Proteins, bcr-abl / genetics
  • Fusion Proteins, bcr-abl / metabolism
  • Gene Expression Regulation, Leukemic* / drug effects
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • MicroRNAs / genetics*
  • Molecular Targeted Therapy
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use
  • RNA Interference*
  • Signal Transduction / drug effects

Substances

  • MicroRNAs
  • Protein Kinase Inhibitors
  • Fusion Proteins, bcr-abl