Advanced glycation end product (AGE)-induced proliferation of HEL cells via receptor for AGE-related signal pathways

Int J Oncol. 2008 Sep;33(3):493-501.

Abstract

This study investigated whether advanced glycation end products (AGE) and RAGE (receptor for AGE) are involved in the proliferation of leukemia cells. AGE strongly induced the proliferation of primary acute myeloid leukemia (AML) cells and cell lines. MAP kinase, PI3K and JAK/STAT pathways were involved in cellular proliferation of HEL cells by AGE. RAGE antisense S-ODN effectively inhibited cell growth, induced apoptosis and reversed AGE-induced expression of targeting molecules in HEL cells. The study demonstrated for the first time that AGE directly induced human AML cell proliferation via the MAPK, PI3K and JAK/STAT pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cell Proliferation*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Flow Cytometry
  • Glycation End Products, Advanced / metabolism*
  • Humans
  • Immunoprecipitation
  • Leukemia, Myeloid, Acute / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • STAT Transcription Factors / metabolism
  • Signal Transduction / physiology*
  • Tumor Cells, Cultured

Substances

  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic
  • STAT Transcription Factors
  • Phosphatidylinositol 3-Kinases
  • Extracellular Signal-Regulated MAP Kinases