Histone deacetylase inhibitors sensitize prostate cancer cells to agents that produce DNA double-strand breaks by targeting Ku70 acetylation.

@article{Chen2007HistoneDI,
  title={Histone deacetylase inhibitors sensitize prostate cancer cells to agents that produce DNA double-strand breaks by targeting Ku70 acetylation.},
  author={C. T. Chen and Y Wang and Hsiao-Ching Yang and P Huang and Samuel K. Kulp and Chih-Cheng Ou Yang and Yen-shen Lu and Shigemi Matsuyama and Ching-Yu Chen and C Chen},
  journal={Cancer research},
  year={2007},
  volume={67 11},
  pages={
          5318-27
        }
}
This study reports a histone deacetylation-independent mechanism whereby histone deacetylase (HDAC) inhibitors sensitize prostate cancer cells to DNA-damaging agents by targeting Ku70 acetylation. Ku70 represents a crucial component of the nonhomologous end joining repair machinery for DNA double-strand breaks (DSB). Our data indicate that pretreatment of prostate cancer cells with HDAC inhibitors (trichostatin A, suberoylanilide hydroxamic acid, MS-275, and OSU-HDAC42) led to increased Ku70… CONTINUE READING

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