Post-transcriptional control of c-myc proto-oncogene expression by glucocorticoid hormones in human T lymphoblastic leukemic cells

Nucleic Acids Res. 1990 Mar 11;18(5):1153-7. doi: 10.1093/nar/18.5.1153.

Abstract

We have studied the regulation of the human c-myc proto-oncogene by glucocorticoid hormones in T lymphoblastic leukemic cells. A significant decrease (50%) of the steady state levels of c-myc mRNA was observed as early as 3 h after dexamethasone treatment of CEM-1.3 human lymphoma cells, reaching less than 5% values, with respect to untreated cells, 24 h after hormone administration. Nuclear run-on experiments showed no modifications of the transcriptional rate from the first exon. However, a slight decrease (15%) of the transcript elongation from the first exon/first intron boundary was observed in the dexamethasone-treated cells. Using actinomycin D to block gene transcription, we have observed a significant increase in the rate of c-myc RNA specific decay after dexamethasone treatment. Furthermore, cycloheximide was able to overcome completely the dexamethasone-induced down-regulation of the c-myc gene expression. Our data suggest that dexamethasone is able to inhibit human c-myc gene expression primarily at the post-transcriptional level, through the synthesis of hormone-induced regulatory protein(s) controlling c-myc transcript stability.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Northern
  • Cycloheximide / pharmacology
  • Dexamethasone / pharmacology*
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Leukemia, T-Cell / genetics*
  • Proto-Oncogene Mas
  • Proto-Oncogenes*
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transcription, Genetic / drug effects*
  • Tumor Cells, Cultured

Substances

  • MAS1 protein, human
  • Proto-Oncogene Mas
  • RNA, Messenger
  • Dexamethasone
  • Cycloheximide