Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability - Institut Curie Accéder directement au contenu
Article Dans Une Revue Frontiers in Cell and Developmental Biology Année : 2021

Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability

Résumé

Breast cancer cells frequently acquire mutations in faithful DNA repair genes, as exemplified by BRCA-deficiency. Moreover, overexpression of an inaccurate DNA repair pathway may also be at the origin of the genetic instability arising during the course of cancer progression. The specific gain in expression of POLQ, encoding the error-prone DNA polymerase Theta (POLθ) involved in theta-mediated end joining (TMEJ), is associated with a characteristic mutational signature. To gain insight into the mechanistic regulation of POLQ expression, this review briefly presents recent findings on the regulation of POLQ in the claudin-low breast tumor subtype, specifically expressing transcription factors involved in epithelial-to-mesenchymal transition (EMT) such as ZEB1 and displaying a paucity in genomic abnormality.
Fichier principal
Vignette du fichier
fcell-09-727429.pdf (823.28 Ko) Télécharger le fichier
Origine : Fichiers éditeurs autorisés sur une archive ouverte
licence : CC BY - Paternité

Dates et versions

hal-03401810 , version 1 (07-06-2023)

Licence

Paternité

Identifiants

Citer

Mélanie K. Prodhomme, Sarah Péricart, Roxane M. Pommier, Anne Pierre Morel, Anne Cécile Brunac, et al.. Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability. Frontiers in Cell and Developmental Biology, 2021, 9, pp.727429. ⟨10.3389/fcell.2021.727429⟩. ⟨hal-03401810⟩
60 Consultations
7 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More