The role of Bcl-XS in radiation sensitivity

M. A. Morgan; J. N. Poynter; J. Maybaum; T. S. Lawrence

doi:10.1667/RR3169

The role of Bcl-X_S in radiation sensitivity

M. A. Morgan, J. N. Poynter, J. Maybaum, T. S. Lawrence

Pediatric Epidemiology & Clinical Research

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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.

Original language	English (US)
Pages (from-to)	535-539
Number of pages	5
Journal	Radiation research
Volume	161
Issue number	5
DOIs	https://doi.org/10.1667/RR3169
State	Published - May 2004

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title = "The role of Bcl-XS in radiation sensitivity",

abstract = "Bcl-XS 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-XS overexpression on radiation sensitivity. Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-XS and reduced the surviving fraction of NIH 3T3 cells to 25%. However, radiation sensitivity was not significantly affected by Bcl-XS expression; the mean inactivation doses for Bcl-XS repressed and Bcl-XS induced cells were 2.7 ± 0.3 and 2.3 ± 0.1 Gy, respectively. We conclude that Bcl-XS 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.",

author = "Morgan, {M. A.} and Poynter, {J. N.} and J. Maybaum and Lawrence, {T. S.}",

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AU - Morgan, M. A.

AU - Poynter, J. N.

AU - Maybaum, J.

AU - Lawrence, T. S.

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N2 - Bcl-XS 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-XS overexpression on radiation sensitivity. Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-XS and reduced the surviving fraction of NIH 3T3 cells to 25%. However, radiation sensitivity was not significantly affected by Bcl-XS expression; the mean inactivation doses for Bcl-XS repressed and Bcl-XS induced cells were 2.7 ± 0.3 and 2.3 ± 0.1 Gy, respectively. We conclude that Bcl-XS 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.

AB - Bcl-XS 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-XS overexpression on radiation sensitivity. Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-XS and reduced the surviving fraction of NIH 3T3 cells to 25%. However, radiation sensitivity was not significantly affected by Bcl-XS expression; the mean inactivation doses for Bcl-XS repressed and Bcl-XS induced cells were 2.7 ± 0.3 and 2.3 ± 0.1 Gy, respectively. We conclude that Bcl-XS 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.

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The role of Bcl-X_S in radiation sensitivity

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