Hypertranscription and replication stress in cancer.
Trends Cancer
; 7(9): 863-877, 2021 09.
Article
in En
| MEDLINE
| ID: mdl-34052137
ABSTRACT
Replication stress results from obstacles to replication fork progression, including ongoing transcription, which can cause transcription-replication conflicts. Oncogenic signaling can promote global increases in transcription activity, also termed hypertranscription. Despite the widely accepted importance of oncogene-induced hypertranscription, its study remains neglected compared with other causes of replication stress and genomic instability in cancer. A growing number of recent studies are reporting that oncogenes, such as RAS, and targeted cancer treatments, such as bromodomain and extraterminal motif (BET) bromodomain inhibitors, increase global transcription, leading to R-loop accumulation, transcription-replication conflicts, and the activation of replication stress responses. Here we discuss our mechanistic understanding of hypertranscription-induced replication stress and the resulting cellular responses, in the context of oncogenes and targeted cancer therapies.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
DNA Replication
/
Neoplasms
Limits:
Humans
Language:
En
Journal:
Trends Cancer
Year:
2021
Document type:
Article
Affiliation country:
United kingdom