MondoA is highly overexpressed in acute lymphoblastic leukemia cells and modulates their metabolism, differentiation and survival

Leuk Res. 2012 Sep;36(9):1185-92. doi: 10.1016/j.leukres.2012.05.009. Epub 2012 Jun 29.

Abstract

Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. To identify novel candidates for targeted therapy, we performed a comprehensive transcriptome analysis identifying MondoA (MLXIP) - a transcription factor regulating glycolysis - to be overexpressed in ALL compared to normal tissues. Using microarray-profiling, gene-set enrichment analysis, RNA interference and functional assays we show that MondoA overexpression increases glucose catabolism and maintains a more immature phenotype, which is associated with enhanced survival and clonogenicity of leukemia cells. These data point to an important contribution of MondoA to leukemia aggressiveness and make MondoA a potential candidate for targeted treatment of ALL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Apoptosis / physiology
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics*
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / metabolism
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / physiology*
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics*
  • Cell Survival / drug effects
  • Cell Survival / genetics
  • Drug Evaluation, Preclinical
  • Gene Expression Profiling
  • Gene Expression Regulation, Leukemic / drug effects
  • Hep G2 Cells
  • Humans
  • Jurkat Cells
  • Microarray Analysis
  • Neoplasm Invasiveness
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology
  • RNA, Small Interfering / pharmacology
  • Tumor Cells, Cultured
  • Up-Regulation / drug effects
  • Up-Regulation / genetics

Substances

  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
  • MLXIP protein, human
  • RNA, Small Interfering