Nucleosome reorganisation in breast cancer tissues.

Breast cancer Chromatin Linker histones Liquid biopsy NRL Nucleosome positioning Nucleosome repeat length Nucleosomics Transcription factors binding cfDNA

Journal

Clinical epigenetics
ISSN: 1868-7083
Titre abrégé: Clin Epigenetics
Pays: Germany
ID NLM: 101516977

Informations de publication

Date de publication:
01 Apr 2024
Historique:
received: 29 12 2023
accepted: 11 03 2024
medline: 2 4 2024
pubmed: 2 4 2024
entrez: 2 4 2024
Statut: epublish

Résumé

Nucleosome repositioning in cancer is believed to cause many changes in genome organisation and gene expression. Understanding these changes is important to elucidate fundamental aspects of cancer. It is also important for medical diagnostics based on cell-free DNA (cfDNA), which originates from genomic DNA regions protected from digestion by nucleosomes. We have generated high-resolution nucleosome maps in paired tumour and normal tissues from the same breast cancer patients using MNase-assisted histone H3 ChIP-seq and compared them with the corresponding cfDNA from blood plasma. This analysis has detected single-nucleosome repositioning at key regulatory regions in a patient-specific manner and common cancer-specific patterns across patients. The nucleosomes gained in tumour versus normal tissue were particularly informative of cancer pathways, with ~ 20-fold enrichment at CpG islands, a large fraction of which marked promoters of genes encoding DNA-binding proteins. The tumour tissues were characterised by a 5-10 bp decrease in the average distance between nucleosomes (nucleosome repeat length, NRL), which is qualitatively similar to the differences between pluripotent and differentiated cells. This effect was correlated with gene activity, differential DNA methylation and changes in local occupancy of linker histone variants H1.4 and H1X. Our study offers a novel resource of high-resolution nucleosome maps in breast cancer patients and reports for the first time the effect of systematic decrease of NRL in paired tumour versus normal breast tissues from the same patient. Our findings provide a new mechanistic understanding of nucleosome repositioning in tumour tissues that can be valuable for patient diagnostics, stratification and monitoring.

Sections du résumé

BACKGROUND BACKGROUND
Nucleosome repositioning in cancer is believed to cause many changes in genome organisation and gene expression. Understanding these changes is important to elucidate fundamental aspects of cancer. It is also important for medical diagnostics based on cell-free DNA (cfDNA), which originates from genomic DNA regions protected from digestion by nucleosomes.
RESULTS RESULTS
We have generated high-resolution nucleosome maps in paired tumour and normal tissues from the same breast cancer patients using MNase-assisted histone H3 ChIP-seq and compared them with the corresponding cfDNA from blood plasma. This analysis has detected single-nucleosome repositioning at key regulatory regions in a patient-specific manner and common cancer-specific patterns across patients. The nucleosomes gained in tumour versus normal tissue were particularly informative of cancer pathways, with ~ 20-fold enrichment at CpG islands, a large fraction of which marked promoters of genes encoding DNA-binding proteins. The tumour tissues were characterised by a 5-10 bp decrease in the average distance between nucleosomes (nucleosome repeat length, NRL), which is qualitatively similar to the differences between pluripotent and differentiated cells. This effect was correlated with gene activity, differential DNA methylation and changes in local occupancy of linker histone variants H1.4 and H1X.
CONCLUSIONS CONCLUSIONS
Our study offers a novel resource of high-resolution nucleosome maps in breast cancer patients and reports for the first time the effect of systematic decrease of NRL in paired tumour versus normal breast tissues from the same patient. Our findings provide a new mechanistic understanding of nucleosome repositioning in tumour tissues that can be valuable for patient diagnostics, stratification and monitoring.

Identifiants

pubmed: 38561804
doi: 10.1186/s13148-024-01656-4
pii: 10.1186/s13148-024-01656-4
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

50

Subventions

Organisme : NIH HHS
ID : Intramural Research Program, National Cancer Institute
Pays : United States
Organisme : Cancer Research UK
ID : EDDPMA-Nov21\100044
Pays : United Kingdom
Organisme : Cancer Research UK
ID : SEBPCTA-2022/100001
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 200733/Z/16/Z
Pays : United Kingdom

Informations de copyright

© 2024. The Author(s).

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Auteurs

Divya R Jacob (DR)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Wilfried M Guiblet (WM)

Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Hulkar Mamayusupova (H)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Mariya Shtumpf (M)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Isabella Ciuta (I)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Luminita Ruje (L)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Svetlana Gretton (S)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
School of Engineering, Arts, Science and Technology, University of Suffolk, James Hehir Building, University Avenue, Ipswich, Suffolk, IP3 0FS, UK.

Milena Bikova (M)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Clark Correa (C)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Emily Dellow (E)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Shivam P Agrawal (SP)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Navid Shafiei (N)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Anastasija Drobysevskaja (A)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Chris M Armstrong (CM)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Jonathan D G Lam (JDG)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Yevhen Vainshtein (Y)

Fraunhofer-Institut für Grenzflächen- und Bioverfahrenstechnik IGB, Nobelstraße 12, 70569, Stuttgart, Germany.

Christopher T Clarkson (CT)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
University College London, Gower St, Bloomsbury, London, WC1E 6BT, UK.

Graeme J Thorn (GJ)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.

Kai Sohn (K)

Fraunhofer-Institut für Grenzflächen- und Bioverfahrenstechnik IGB, Nobelstraße 12, 70569, Stuttgart, Germany.

Madapura M Pradeepa (MM)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, E1 2AT, UK.

Sankaran Chandrasekharan (S)

Colchester General Hospital, East Suffolk and North Essex NHS Foundation Trust, Turner Road, Colchester, CO4 5JL, UK.

Greg N Brooke (GN)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Elena Klenova (E)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.

Victor B Zhurkin (VB)

Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. zhurkin@nih.gov.

Vladimir B Teif (VB)

School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK. vteif@essex.ac.uk.

Classifications MeSH