BRCA1 deficiency in triple-negative breast cancer: Protein stability as a basis for therapy
- 주제(키워드) BRCA1 deficiency , Chemotherapy resistance , Multifunction , Proteasomal degradation , Triple-negative breast cancer
- 등재 SCIE, SCOPUS
- OA유형 hybrid
- 발행기관 Elsevier Masson s.r.l.
- 발행년도 2023
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000203337
- 본문언어 영어
- Published As https://doi.org/10.1016/j.biopha.2022.114090
- PubMed https://pubmed.ncbi.nlm.nih.gov/36493696
초록/요약
Mutations in breast cancer-associated 1 (BRCA1) increase the lifetime risk of developing breast cancer by up to 51% over the risk of the general population. Many aspects of this multifunctional protein have been revealed, including its essential role in homologous recombination repair, E3 ubiquitin ligase activity, transcriptional regulation, and apoptosis. Although most studies have focused on BRCA1 deficiency due to mutations, only a minority of patients carry BRCA1 mutations. A recent study has suggested an expanded definition of BRCA1 deficiency with reduced BRCA1 levels, which accounts for almost half of all triple-negative breast cancer (TNBC) patients. Reduced BRCA1 levels can result from epigenetic modifications or increased proteasomal degradation. In this review, we discuss how this knowledge of BRCA1 function and regulation of BRCA1 protein stability can help overcome the challenges encountered in the clinic and advance current treatment strategies for BRCA1-related breast cancer patients, especially focusing on TNBC. © 2022 The Authors
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