Regulation of TNF-alpha and IL-1 gene expression during TPA-induced differentiation of "Malignant histiocytosis" DEL cell line t(5;6) (q35:p21)

Anticancer Res. 1996 Jan-Feb;16(1):455-60.

Abstract

The production of TNF-alpha and IL-1 alpha and beta molecules has been shown to be associated with the proliferation and activation of cells of the monocyte/macrophage series, the intermediate steps in the synthesis of these molecules have been less investigated. Unstimulated and TPA stimulated DEL cells (a CD30-positive, t(5;6)(q35;p21) malignant histiocytosis cell line) were used to study the expression of TNF-alpha and IL-1 genes and to evaluate, by nuclear run-on assay and biological measurements, the control of their transcription and the level of protein production. To refine this analysis, the effects of cycloheximide and actinomycin D were also evaluated in this investigation. Following TPA stimulation, transcription of TNF-alpha (constitutively present) increased threefold as early as 30 mins and started decreasing by 24h. Cycloheximide superinduced the expression of TNF-alpha mRNA and, accordingly, the release of its protein. By contrast, transcription of IL-1 molecules appeared de novo and did not result in a biologically detectable protein. Measurements of RNA half line after actinomycin D indicated that TNF-a and IL-1 alpha mRNAs are not as stable as that of IL-1 beta. These results indicate that, despite their common synergistic activity, the transcriptional and post-transcriptional mechanisms regulating the synthesis of TNF-alpha and IL-1 alpha and IL-1 beta involve different pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Northern
  • Cell Differentiation / drug effects
  • Chromosomes, Human, Pair 5
  • Chromosomes, Human, Pair 6
  • Cycloheximide / pharmacology
  • Cytoplasm / metabolism
  • Drug Stability
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Histiocytic Sarcoma / drug therapy*
  • Histiocytic Sarcoma / genetics*
  • Histiocytic Sarcoma / pathology
  • Humans
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / genetics*
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger / metabolism
  • Tetradecanoylphorbol Acetate / pharmacology*
  • Transcription, Genetic
  • Translocation, Genetic
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • Interleukin-1
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Cycloheximide
  • Tetradecanoylphorbol Acetate