Tumor necrosis factor-induced interleukin-6 expression and cytotoxicity follow a common signal transduction pathway in L929 cells

Biochem Biophys Res Commun. 1991 Aug 15;178(3):993-1001. doi: 10.1016/0006-291x(91)90990-o.

Abstract

Interleukin (IL)-6 gene induction was studied in response to treatment with Tumor Necrosis Factor (TNF) in the sensitive murine L929 cell line. Under conditions where TNF-mediated cytotoxicity was either increased or decreased, depending on addition of activators or inhibitors, we found that the TNF-induced IL6 gene expression was likewise enhanced or repressed. We conclude that the signal (or part of the signals) going to the nucleus and responsible for gene activation is conducted along the reaction mechanism leading to cellular toxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cell Line
  • Cell Survival / drug effects
  • Fibrosarcoma
  • Gene Expression / drug effects
  • Interleukin-6 / genetics*
  • L Cells / cytology
  • L Cells / drug effects
  • L Cells / immunology
  • Mice
  • Nucleic Acid Hybridization
  • RNA / genetics
  • RNA / isolation & purification
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics*
  • Sarcoma, Experimental
  • Signal Transduction / drug effects*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-6
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • RNA