[Analysis of the methylation in the promoter of LRP15 gene and its expression]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2005 Apr;13(2):188-91.
[Article in Chinese]

Abstract

To study the methylation in the promoter of LRP15 gene and its relationship with gene expression and to explore the possible mechanism of regulating LRP15 gene methylation, the methylation in the promoter of LRP15 gene in K562 cell line was detected by MS-PCR. Then K562 was exposed to 5-aza-2'-deoxycytidine (CdR) and trichostatin (TSA), to determine whether the silencing of LRP15 gene by de novo methylation could be reversed. As a result, it was confirmed by MS-PCR that the promoter of LRP15 was hypermathylated in K562 cell line, and lost its transcription activity. After CdR, with or without TSA, the silencing of LRP15 gene by de novo methylation can be reversed. Observation demonstrated that the expression of LRP15 was controlled by methylation in its promoter in K562. It is suggested that methyltransferase inhibitor and deacetylase inhibitor may be effective agents in leukemia therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Azacitidine / analogs & derivatives
  • Azacitidine / pharmacology
  • DNA Methylation*
  • DNA Modification Methylases / antagonists & inhibitors
  • Decitabine
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation / drug effects
  • Histone Deacetylase Inhibitors
  • Humans
  • Hydroxamic Acids / pharmacology
  • K562 Cells
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics*
  • Polymerase Chain Reaction / methods
  • Promoter Regions, Genetic / genetics*

Substances

  • Enzyme Inhibitors
  • Histone Deacetylase Inhibitors
  • Hydroxamic Acids
  • LRRC3B protein, human
  • Neoplasm Proteins
  • trichostatin A
  • Decitabine
  • DNA Modification Methylases
  • Azacitidine