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

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 ex...

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Published in:Frontiers in cell and developmental biology 2021-08, Vol.9, p.727429-727429
Main Authors: Prodhomme, Mélanie K., Péricart, Sarah, Pommier, Roxane M., Morel, Anne-Pierre, Brunac, Anne-Cécile, Franchet, Camille, Moyret-Lalle, Caroline, Brousset, Pierre, Puisieux, Alain, Hoffmann, Jean-Sébastien, Tissier, Agnès
Format: Article
Language:English
Subjects:
Biochemistry, Molecular Biology
Cancer
Cell and Developmental Biology
DNA polymerase theta
DNA Repair
epithelial to mesenchymal transition
Genomics
Life Sciences
replicative stress
TMEJ
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Summary: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.
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2021.727429