Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression

Cancer Cell. 2008 Jun;13(6):496-506. doi: 10.1016/j.ccr.2008.04.018.

Abstract

The mammalian genome contains several hundred microRNAs that regulate gene expression through modulation of target mRNAs. Here, we report a fragile chromosomal region lost in specific hematopoietic malignancies. This 7 Mb region encodes about 12% of all genomic microRNAs, including miR-203. This microRNA is additionally hypermethylated in several hematopoietic tumors, including chronic myelogenous leukemias and some acute lymphoblastic leukemias. A putative miR-203 target, ABL1, is specifically activated in these hematopoietic malignancies in some cases as a BCR-ABL1 fusion protein (Philadelphia chromosome). Re-expression of miR-203 reduces ABL1 and BCR-ABL1 fusion protein levels and inhibits tumor cell proliferation in an ABL1-dependent manner. Thus, miR-203 functions as a tumor suppressor, and re-expression of this microRNA might have therapeutic benefits in specific hematopoietic malignancies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions
  • Animals
  • Azacitidine / pharmacology
  • Cell Line, Tumor
  • Cell Proliferation* / drug effects
  • Chromosomes, Human, Pair 14
  • Chromosomes, Mammalian
  • DNA Methylation*
  • DNA Modification Methylases / antagonists & inhibitors
  • DNA Modification Methylases / metabolism
  • Enzyme Inhibitors / pharmacology
  • Fusion Proteins, bcr-abl / metabolism*
  • Gene Expression Profiling
  • Gene Expression Regulation, Leukemic
  • Gene Expression Regulation, Neoplastic* / drug effects
  • Gene Silencing*
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Loss of Heterozygosity
  • Lymphoma, T-Cell / genetics
  • Lymphoma, T-Cell / metabolism
  • Lymphoma, T-Cell / pathology
  • Lymphoproliferative Disorders / enzymology
  • Lymphoproliferative Disorders / genetics
  • Lymphoproliferative Disorders / metabolism*
  • Lymphoproliferative Disorders / pathology
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Phenylbutyrates / pharmacology
  • Philadelphia Chromosome
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins c-abl / metabolism*
  • Time Factors
  • Transfection
  • Up-Regulation
  • Whole-Body Irradiation

Substances

  • 3' Untranslated Regions
  • Enzyme Inhibitors
  • MicroRNAs
  • Phenylbutyrates
  • abl-bcr fusion protein, human
  • 4-phenylbutyric acid
  • DNA Modification Methylases
  • Fusion Proteins, bcr-abl
  • Proto-Oncogene Proteins c-abl
  • Azacitidine

Associated data

  • GEO/GSE10858
  • GEO/GSE10859
  • GEO/GSE10861