Background: The mechanism by which heat sensitizes mammalian cells to ionizing radiation remains to be elucidated. We determined whether base excision repair (BER) is involved in heat-radiosensitization and report novel findings that provide insight regarding the role of BER in the radiation response of HeLa cells. Materials and Methods: An siRNA approach was utilized to suppress expression of AP endonuclease (Apel), a critical enzyme of BER. Clonogenic survival curves were obtained for HeLa cells expressing normal or reduced Apel content and which had been irradiated, and these were compared to survival curves from cells that were irradiated prior to hyperthermia treatment. Results: The amount of heat-radiosensitization observed in Apel-suppressed cells was similar to or slightly greater than that observed in cells expressing near-normal levels of Apel. Interestingly, we also found that for unheated HeLa cells, suppressed expression of Apel resulted in enhanced resistance to X-rays. Conclusion: The data suggest that Apel, and therefore BER, is not involved in heat-radiosensitization. However, the observation that suppressed expression of Apel results in enhanced radioresistance supports the notion that BER may be detrimental to the survival of irradiated cells.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Apr 1 2009|
- Dna repair
ASJC Scopus subject areas
- Cancer Research