Suppression of c-myc is a critical step in glucocorticoid-induced human leukemic cell lysis

J Biol Chem. 1993 Aug 25;268(24):18306-12.

Abstract

Glucocorticoids evoke cytolysis in clonal human leukemic CEM-C7 cells. Suppression of c-myc mRNA by dexamethasone closely correlates with cell lysis only in CEM clones with both glucocorticoid receptor and intact lysis functions. We tested the theory that c-myc repression is essential for glucocorticoid-induced lymphocytolysis by preventing down-regulation of c-myc gene in the presence of dexamethasone and by reducing c-myc mRNA levels with antisense oligonucleotides. We find that sustained expression of c-myc provides resistance to dexamethasone-induced lysis, and antisense c-myc oligomers induce cell lysis. The lethal effects of dexamethasone in these leukemic cells appear to involve reduction of c-myc below the levels required to maintain cellular growth and integrity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Base Sequence
  • Cell Death / drug effects
  • Cell Survival / drug effects*
  • Dexamethasone / pharmacology*
  • Drug Resistance / genetics
  • Exons
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Genes, myc*
  • Genetic Vectors
  • Humans
  • Kinetics
  • Leukemia
  • Mammary Tumor Virus, Mouse / genetics
  • Mice
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides / pharmacology
  • Oligonucleotides, Antisense / pharmacology*
  • Proto-Oncogene Proteins c-myc / biosynthesis
  • RNA, Messenger / metabolism
  • Transcription, Genetic / drug effects
  • Transfection
  • Tumor Cells, Cultured
  • Zinc / pharmacology

Substances

  • Oligodeoxyribonucleotides
  • Oligonucleotides, Antisense
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • Dexamethasone
  • Zinc