Acetylation: A novel link between double-strand break repair and autophagy

Ghadeer Shubassi, Thomas Robert, Fabio Vanoli, Saverio Minucci, Marco Foiani

Research output: Contribution to journalArticlepeer-review


Histone deacetylase (HDAC) inhibitors are clinically relevant because they are used as anticancer drugs. Recent evidence sheds light on an intriguing connection among the DNA damage response (DDR), protein acetylation, and autophagy. HDAC inhibitors have been shown to counteract key steps in the cellular response to double-strand break formation by affecting checkpoint activation, homologous recombination-mediated repair of DNA lesions, and stability of crucial enzymes involved in resection of DNA ends. The degradation of the resection factors depends on autophagy, which plays a detrimental role when cells are in a hyperacetylated state and experience treatment with radiomimetic anticancer drugs. Future work will be required to further investigate the mechanisms underlying the link between acetylation, autophagy, and the DDR, as well as the significance of mTORC1 inhibitors, which are potent inducers of autophagy that are now used in cancer treatment.

Original languageEnglish
Pages (from-to)1332-1335
Number of pages4
JournalCancer Research
Issue number6
Publication statusPublished - Mar 15 2012

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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