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Breast Cancer Research
Published in: Breast Cancer Research 1/2020

01-12-2020 | Breast Cancer | Research article

Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer

Authors: Laura A. Baker, Holly Holliday, Daniel Roden, Christoph Krisp, Sunny Z. Wu, Simon Junankar, Aurelien A. Serandour, Hisham Mohammed, Radhika Nair, Geetha Sankaranarayanan, Andrew M. K. Law, Andrea McFarland, Peter T. Simpson, Sunil Lakhani, Eoin Dodson, Christina Selinger, Lyndal Anderson, Goli Samimi, Neville F. Hacker, Elgene Lim, Christopher J. Ormandy, Matthew J. Naylor, Kaylene Simpson, Iva Nikolic, Sandra O’Toole, Warren Kaplan, Mark J. Cowley, Jason S. Carroll, Mark Molloy, Alexander Swarbrick

Published in: Breast Cancer Research | Issue 1/2020

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Abstract

Background

Basal-like breast cancer (BLBC) is a poorly characterised, heterogeneous disease. Patients are diagnosed with aggressive, high-grade tumours and often relapse with chemotherapy resistance. Detailed understanding of the molecular underpinnings of this disease is essential to the development of personalised therapeutic strategies. Inhibitor of differentiation 4 (ID4) is a helix-loop-helix transcriptional regulator required for mammary gland development. ID4 is overexpressed in a subset of BLBC patients, associating with a stem-like poor prognosis phenotype, and is necessary for the growth of cell line models of BLBC through unknown mechanisms.

Methods

Here, we have defined unique molecular insights into the function of ID4 in BLBC and the related disease high-grade serous ovarian cancer (HGSOC), by combining RIME proteomic analysis, ChIP-seq mapping of genomic binding sites and RNA-seq.

Results

These studies reveal novel interactions with DNA damage response proteins, in particular, mediator of DNA damage checkpoint protein 1 (MDC1). Through MDC1, ID4 interacts with other DNA repair proteins (γH2AX and BRCA1) at fragile chromatin sites. ID4 does not affect transcription at these sites, instead binding to chromatin following DNA damage. Analysis of clinical samples demonstrates that ID4 is amplified and overexpressed at a higher frequency in BRCA1-mutant BLBC compared with sporadic BLBC, providing genetic evidence for an interaction between ID4 and DNA damage repair deficiency.

Conclusions

These data link the interactions of ID4 with MDC1 to DNA damage repair in the aetiology of BLBC and HGSOC.
Appendix
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Metadata
Title
Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer
Authors
Laura A. Baker
Holly Holliday
Daniel Roden
Christoph Krisp
Sunny Z. Wu
Simon Junankar
Aurelien A. Serandour
Hisham Mohammed
Radhika Nair
Geetha Sankaranarayanan
Andrew M. K. Law
Andrea McFarland
Peter T. Simpson
Sunil Lakhani
Eoin Dodson
Christina Selinger
Lyndal Anderson
Goli Samimi
Neville F. Hacker
Elgene Lim
Christopher J. Ormandy
Matthew J. Naylor
Kaylene Simpson
Iva Nikolic
Sandra O’Toole
Warren Kaplan
Mark J. Cowley
Jason S. Carroll
Mark Molloy
Alexander Swarbrick
Publication date
01-12-2020
Publisher
BioMed Central
Published in
Breast Cancer Research / Issue 1/2020
Electronic ISSN: 1465-542X
DOI
https://doi.org/10.1186/s13058-020-01306-6

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