Suppression of antiproliferative effects of tumor necrosis factor by transfection of cells with human platelet-derived growth factor B/c-sis gene

FEBS Lett. 1995 Jan 2;357(1):1-6. doi: 10.1016/0014-5793(94)01299-g.

Abstract

The growth of cells is determined by the balance between growth-stimulatory and growth-inhibitory signals. In the present study, we demonstrate that the transfection of NIH 3T3 cells with a platelet-derived growth factor (PDGF-Blc-sis) gene induces resistance to the anticellular effects of tumor necrosis factor (TNF). Human tumor cell lines that express elevated levels of c-sis (e.g. epidermoid carcinoma, A-431) are also TNF resistant, whereas those that express no significant levels of this gene (e.g. breast adenocarcinoma, MCF-7) are TNF sensitive. Transfection of cells with the c-sis gene leads to down-modulation of TNF receptors and also a decrease in intracellular glutathione levels. Thus, our results demonstrate that over-expression of PDGF-Blc-sis by certain tumor cells can lead to their protection from the anticellular effects of TNF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Division / physiology*
  • Glutathione / metabolism
  • Humans
  • Interferon-gamma / pharmacology
  • Mice
  • Platelet-Derived Growth Factor / genetics
  • Platelet-Derived Growth Factor / physiology*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-sis
  • Receptors, Tumor Necrosis Factor / metabolism
  • Transfection
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Platelet-Derived Growth Factor
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-sis
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Glutathione