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Epigenetic changes in histone acetylation underpin resistance to the topoisomerase I inhibitor irinotecan.

Abstract：

:The topoisomerase I (TOP1) inhibitor irinotecan triggers cell death by trapping TOP1 on DNA, generating cytotoxic protein-linked DNA breaks (PDBs). Despite its wide application in a variety of solid tumors, the mechanisms of cancer cell resistance to irinotecan remains poorly understood. Here, we generated colorectal cancer (CRC) cell models for irinotecan resistance and report that resistance is neither due to downregulation of the main cellular target of irinotecan TOP1 nor upregulation of the key TOP1 PDB repair factor TDP1. Instead, the faster repair of PDBs underlies resistance, which is associated with perturbed histone H4K16 acetylation. Subsequent treatment of irinotecan-resistant, but not parental, CRC cells with histone deacetylase (HDAC) inhibitors can effectively overcome resistance. Immunohistochemical analyses of CRC tissues further corroborate the importance of histone H4K16 acetylation in CRC. Finally, the resistant clones exhibit cross-resistance with oxaliplatin but not with ionising radiation or 5-fluoruracil, suggesting that the latter two could be employed following loss of irinotecan response. These findings identify perturbed chromatin acetylation in irinotecan resistance and establish HDAC inhibitors as potential therapeutic means to overcome resistance.

journal_name

Nucleic Acids Res

journal_title

Nucleic acids research

authors

Meisenberg C,Ashour ME,El-Shafie L,Liao C,Hodgson A,Pilborough A,Khurram SA,Downs JA,Ward SE,El-Khamisy SF

doi

10.1093/nar/gkw1026

subject

Has Abstract

pub_date

2017-02-17 00:00:00

pages

1159-1176

issue

3

eissn

0305-1048

issn

1362-4962

pii

2333920

journal_volume

45

pub_type

杂志文章

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