MYC as a driver of stochastic chromatin networks: implications for the fitness of cancer cells.


Journal

Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011

Informations de publication

Date de publication:
04 11 2020
Historique:
accepted: 11 10 2020
revised: 09 09 2020
received: 09 07 2020
pubmed: 15 10 2020
medline: 21 11 2020
entrez: 14 10 2020
Statut: ppublish

Résumé

The relationship between stochastic transcriptional bursts and dynamic 3D chromatin states is not well understood. Using an innovated, ultra-sensitive technique, we address here enigmatic features underlying the communications between MYC and its enhancers in relation to the transcriptional process. MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells. Dynamic encounters with pathologically activated enhancers responsive to a range of environmental cues, involved <10% of active MYC alleles at any given time in colon cancer cells. Being the most central node of the chromatin network, MYC itself likely drives its communications with flanking enhancers, rather than vice versa. We submit that these features underlie an acquired ability of MYC to become dynamically activated in response to a diverse range of environmental cues encountered by the cell during the neoplastic process.

Identifiants

pubmed: 33051686
pii: 5922798
doi: 10.1093/nar/gkaa817
pmc: PMC7641766
doi:

Substances chimiques

Proto-Oncogene Proteins c-myc 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

10867-10876

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.

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Auteurs

Noriyuki Sumida (N)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

Emmanouil G Sifakis (EG)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

Narsis A Kiani (NA)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

Anna Lewandowska Ronnegren (AL)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

Barbara A Scholz (BA)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

Johanna Vestlund (J)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Unit of Computational Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, L8:05, SE-171 76, Stockholm, Sweden.

David Gomez-Cabrero (D)

Unit of Computational Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, L8:05, SE-171 76, Stockholm, Sweden.
Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 9RT, UK.

Jesper Tegner (J)

Unit of Computational Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, L8:05, SE-171 76, Stockholm, Sweden.
Science for Life Laboratory, Tomtebodavägen 23A, SE-17165, Solna, Sweden.
Biological and Environmental Sciences and Engineering Division, Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia.

Anita Göndör (A)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

Rolf Ohlsson (R)

Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.

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