Enhanced radiosensitivity by inhibition of nuclear factor kappa B activation in human malignant glioma cells

Int J Radiat Biol. 1997 Aug;72(2):157-62. doi: 10.1080/095530097143374.


To clarify the relationship between cellular radiosensitivity and nuclear factor kappa B (NF-kappa B) activation, an expression plasmid was constructed for I kappa B-alpha, a cellular inhibitory protein of NF-kappa B, and transfected it into two human malignant glioma cell lines. Cells overexpressing the I kappa B-alpha protein were more radiosensitive than the parental cells and one transfected clone with low expression. In the parental cell lines and one transfected clone with low expression, the sequence specific DNA-binding activity of NF-kappa B was considerably increased between 1 and 2 h after irradiation. In contrast, no increase in the DNA-binding activity was observed in the transfected clone overexpressing I kappa B-alpha protein. These results suggest that the activation of NF-kappa B may be one of the intrinsic responses determining cellular radiosensitivity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Clone Cells / radiation effects
  • DNA / metabolism
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / pharmacology*
  • Glioma / metabolism*
  • Humans
  • I-kappa B Proteins*
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • RNA, Messenger / metabolism
  • Radiation Tolerance / drug effects*
  • Tumor Cells, Cultured


  • DNA-Binding Proteins
  • I-kappa B Proteins
  • NF-kappa B
  • NFKBIA protein, human
  • RNA, Messenger
  • NF-KappaB Inhibitor alpha
  • DNA