HDAC4 and HDAC6 sustain DNA double strand break repair and stem-like phenotype by promoting radioresistance in glioblastoma cells.

@article{Marampon2017HDAC4AH,
  title={HDAC4 and HDAC6 sustain DNA double strand break repair and stem-like phenotype by promoting radioresistance in glioblastoma cells.},
  author={Francesco Marampon and Francesca Megiorni and Simona Camero and Clara Crescioli and Heather Prudence McDowell and Roberta Sferra and Antonella Vetuschi and Simona Pompili and Luca Ventura and Francesca De Felice and Vincenzo Tombolini and Carlo Dominici and Roberto Maggio and Claudio Festuccia and Giovanni Luca Gravina},
  journal={Cancer letters},
  year={2017},
  volume={397},
  pages={1-11}
}
The role of histone deacetylase (HDAC) 4 and 6 in glioblastoma (GBM) radioresistance was investigated. We found that tumor samples from 31 GBM patients, who underwent temozolomide and radiotherapy combined treatment, showed HDAC4 and HDAC6 expression in 93.5% and 96.7% of cases, respectively. Retrospective clinical data analysis demonstrated that high-intensity HDAC4 and/or HDAC6 immunostaining was predictive of poor clinical outcome. In vitro experiments revealed that short hairpin RNA… CONTINUE READING
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