E2F1: Cause and Consequence of DNA Replication Stress.
DNA replication stress
E2F1
cyclin E
cyclin F
retinoblastoma
ribonucleotide reductase
ubiquitin proteasome system
Journal
Frontiers in molecular biosciences
ISSN: 2296-889X
Titre abrégé: Front Mol Biosci
Pays: Switzerland
ID NLM: 101653173
Informations de publication
Date de publication:
2020
2020
Historique:
received:
27
08
2020
accepted:
30
11
2020
entrez:
5
3
2021
pubmed:
6
3
2021
medline:
6
3
2021
Statut:
epublish
Résumé
In mammalian cells, cell cycle entry occurs in response to the correct stimuli and is promoted by the transcriptional activity of E2F family members. E2F proteins regulate the transcription of S phase cyclins and genes required for DNA replication, DNA repair, and apoptosis. The activity of E2F1, the archetypal and most heavily studied E2F family member, is tightly controlled by the DNA damage checkpoints to modulate cell cycle progression and initiate programmed cell death, when required. Altered tumor suppressor and oncogenic signaling pathways often result in direct or indirect interference with E2F1 regulation to ensure higher rates of cell proliferation independently of external cues. Despite a clear link between dysregulated E2F1 activity and cancer progression, literature on the contribution of E2F1 to DNA replication stress phenotypes is somewhat scarce. This review discusses how dysfunctional tumor suppressor and oncogenic signaling pathways promote the disruption of E2F1 transcription and hence of its transcriptional targets, and how such events have the potential to drive DNA replication stress. In addition to the involvement of E2F1 upstream of DNA replication stress, this manuscript also considers the role of E2F1 as a downstream effector of the response to this type of cellular stress. Lastly, the review introduces some reflections on how E2F1 activity is integrated with checkpoint control through post-translational regulation, and proposes an exploitable tumor weakness based on this axis.
Identifiants
pubmed: 33665206
doi: 10.3389/fmolb.2020.599332
pmc: PMC7921158
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
599332Subventions
Organisme : Medical Research Council
ID : MC_UU_00001/7
Pays : United Kingdom
Informations de copyright
Copyright © 2021 Fouad, Hauton and D'Angiolella.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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