The role of Bcl-X(S) in radiation sensitivity

Radiat Res. 2004 May;161(5):535-9. doi: 10.1667/rr3169.

Abstract

Bcl-X(S) is a pro-apoptosis member of the Bcl2 family that has been shown to induce cell death and enhance chemosensitivity. We have investigated the effect of Bcl-X(S) overexpression on radiation sensitivity. Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-X(S) and reduced the surviving fraction of NIH 3T3 cells to 25%. However, radiation sensitivity was not significantly affected by Bcl-X(S) expression; the mean inactivation doses for Bcl-X(S) repressed and Bcl-X(S) induced cells were 2.7 +/- 0.3 and 2.3 +/- 0.1 Gy, respectively. We conclude that Bcl-X(S) induces cell death without affecting radiation sensitivity. These results suggest that mitochondrial pathways to apoptosis may not have a significant role in survival after irradiation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Apoptosis / radiation effects*
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • Dose-Response Relationship, Radiation
  • Mice
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Radiation Dosage
  • Radiation Tolerance / drug effects
  • Radiation Tolerance / physiology*
  • Radiation Tolerance / radiation effects*
  • Tetracycline / pharmacology
  • bcl-X Protein

Substances

  • Bcl2l1 protein, mouse
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-X Protein
  • Tetracycline