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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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2021-08-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2021.727429/full |
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| author | Mélanie K. Prodhomme Mélanie K. Prodhomme Sarah Péricart Roxane M. Pommier Anne-Pierre Morel Anne-Pierre Morel Anne-Cécile Brunac Camille Franchet Caroline Moyret-Lalle Caroline Moyret-Lalle Pierre Brousset Alain Puisieux Alain Puisieux Jean-Sébastien Hoffmann Agnès Tissier Agnès Tissier |
| author_facet | Mélanie K. Prodhomme Mélanie K. Prodhomme Sarah Péricart Roxane M. Pommier Anne-Pierre Morel Anne-Pierre Morel Anne-Cécile Brunac Camille Franchet Caroline Moyret-Lalle Caroline Moyret-Lalle Pierre Brousset Alain Puisieux Alain Puisieux Jean-Sébastien Hoffmann Agnès Tissier Agnès Tissier |
| author_sort | Mélanie K. Prodhomme |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-22T16:04:50Z |
| format | Article |
| id | doaj.art-62d2634ad0974109888f7e46b74d8f22 |
| institution | Directory Open Access Journal |
| issn | 2296-634X |
| language | English |
| last_indexed | 2024-12-22T16:04:50Z |
| publishDate | 2021-08-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj.art-62d2634ad0974109888f7e46b74d8f222022-12-21T18:20:37ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-08-01910.3389/fcell.2021.727429727429Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome StabilityMélanie K. Prodhomme0Mélanie K. Prodhomme1Sarah Péricart2Roxane M. Pommier3Anne-Pierre Morel4Anne-Pierre Morel5Anne-Cécile Brunac6Camille Franchet7Caroline Moyret-Lalle8Caroline Moyret-Lalle9Pierre Brousset10Alain Puisieux11Alain Puisieux12Jean-Sébastien Hoffmann13Agnès Tissier14Agnès Tissier15INSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Équipe Labellisée Ligue Contre le Cancer, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, FranceLabEx DEVweCAN, Université de Lyon, Lyon, FranceLaboratoire d’Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Toulouse, FranceGilles Thomas Bioinformatics Platform, Centre Léon Bérard, Cancer Research Centre of Lyon, Lyon, FranceINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Équipe Labellisée Ligue Contre le Cancer, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, FranceLabEx DEVweCAN, Université de Lyon, Lyon, FranceLaboratoire d’Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Toulouse, FranceLaboratoire d’Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Toulouse, FranceINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Équipe Labellisée Ligue Contre le Cancer, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, FranceLabEx DEVweCAN, Université de Lyon, Lyon, FranceLaboratoire d’Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Toulouse, FranceINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Équipe Labellisée Ligue Contre le Cancer, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, FranceInstitut Curie, Versailles Saint-Quentin-en-Yvelines University, PSL Research University, Paris, FranceLaboratoire d’Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Toulouse, FranceINSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Centre of Lyon, Équipe Labellisée Ligue Contre le Cancer, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, FranceLabEx DEVweCAN, Université de Lyon, Lyon, FranceBreast 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.https://www.frontiersin.org/articles/10.3389/fcell.2021.727429/fullepithelial to mesenchymal transitionDNA RepairTMEJDNA polymerase thetareplicative stress |
| spellingShingle | Mélanie K. Prodhomme Mélanie K. Prodhomme Sarah Péricart Roxane M. Pommier Anne-Pierre Morel Anne-Pierre Morel Anne-Cécile Brunac Camille Franchet Caroline Moyret-Lalle Caroline Moyret-Lalle Pierre Brousset Alain Puisieux Alain Puisieux Jean-Sébastien Hoffmann Agnès Tissier Agnès Tissier Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability Frontiers in Cell and Developmental Biology epithelial to mesenchymal transition DNA Repair TMEJ DNA polymerase theta replicative stress |
| title | Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability |
| title_full | Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability |
| title_fullStr | Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability |
| title_full_unstemmed | Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability |
| title_short | Opposite Roles for ZEB1 and TMEJ in the Regulation of Breast Cancer Genome Stability |
| title_sort | opposite roles for zeb1 and tmej in the regulation of breast cancer genome stability |
| topic | epithelial to mesenchymal transition DNA Repair TMEJ DNA polymerase theta replicative stress |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2021.727429/full |
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