Abstract
Basal-like breast cancer (BLBC) and triple-negative breast cancer (TNBC) are aggressive forms of human breast cancer with poor prognosis and limited treatment response. Molecular understanding of BLBC and TNBC biology is instrumental to improve detection and management of these deadly diseases. Tumor suppressors WW domain-containing oxidoreductase (WWOX) and TP53 are altered in BLBC and in TNBC. Nevertheless, the functional interplay between WWOX and p53 is poorly understood. In a recent study by Abdeen and colleagues, it has been demonstrated that WWOX loss drives BLBC formation via deregulating p53 functions. In this review, we highlight important signaling pathways regulated by WWOX and p53 that are related to estrogen receptor signaling, epithelial-to-mesenchymal transition, and genomic instability and how they impact BLBC and TNBC development.
| Original language | English |
|---|---|
| Pages (from-to) | 1177-1186 |
| Number of pages | 10 |
| Journal | Cell Cycle |
| Volume | 18 |
| Issue number | 11 |
| DOIs | |
| State | Published - 3 Jun 2019 |
Bibliographical note
Funding Information:The Aqeilan lab is supported by European Research Council (ERC)-Consolidator Grant under the European Union’s Horizon 2020 research and innovation program (grant agreement No. 682118) and Israel Science Foundation (grant agreement No 1574/15).
Funding Information:
This work was supported by the FP7 Ideas: European Research Council [682118]; Israel Science Foundation [1574/15]. The Aqeilan lab is supported by European Research Council (ERC)-Consolidator Grant under the European Union?s Horizon 2020 research and innovation program (grant agreement No. 682118) and Israel Science Foundation (grant agreement No 1574/15).
Publisher Copyright:
© 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.
Keywords
- BLBC
- ER
- TNBC
- breast cancer
- fragile site
- genomic instability
