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Enhanced DNA damage response through RAD50 in triple negative breast cancer resistant and cancer stem-like cells contributes to chemoresistance
E. Abad, L. Civit, D. Potesil, Z. Zdrahal, A. Lyakhovich
Language English Country Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 2005 to 1 year ago
Medline Complete (EBSCOhost)
from 2005-01-01 to 1 year ago
Wiley Free Content
from 2005 to 1 year ago
PubMed
33090711
DOI
10.1111/febs.15588
Knihovny.cz E-resources
- MeSH
- Drug Resistance, Neoplasm drug effects genetics MeSH
- Cisplatin administration & dosage MeSH
- Cyclophosphamide administration & dosage MeSH
- DNA-Binding Proteins genetics MeSH
- Doxorubicin administration & dosage MeSH
- DNA Repair Enzymes genetics MeSH
- MRE11 Homologue Protein genetics MeSH
- Acid Anhydride Hydrolases genetics MeSH
- Nuclear Proteins genetics MeSH
- Humans MeSH
- Neoplastic Stem Cells drug effects metabolism MeSH
- DNA Damage drug effects MeSH
- Disease-Free Survival MeSH
- Cell Cycle Proteins genetics MeSH
- Triple Negative Breast Neoplasms drug therapy genetics MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
A growing body of evidence supports the notion that cancer resistance is driven by a small subset of cancer stem cells (CSC), responsible for tumor initiation, growth, and metastasis. Both CSC and chemoresistant cancer cells may share common qualities to activate a series of self-defense mechanisms against chemotherapeutic drugs. Here, we aimed to identify proteins in chemoresistant triple-negative breast cancer (TNBC) cells and corresponding CSC-like spheroid cells that may contribute to their resistance. We have identified several candidate proteins representing the subfamilies of DNA damage response (DDR) system, the ATP-binding cassette, and the 26S proteasome degradation machinery. We have also demonstrated that both cell types exhibit enhanced DDR when compared to corresponding parental counterparts, and identified RAD50 as one of the major contributors in the resistance phenotype. Finally, we have provided evidence that depleting or blocking RAD50 within the Mre11-Rad50-NBS1 (MRN) complex resensitizes CSC and chemoresistant TNBC cells to chemotherapeutic drugs.
Department of Experimental and Health Sciences Universitat Pompeu Fabra Barcelona Spain
National Centre for Biomolecular Research Faculty of Science Masaryk University Brno Czech Republic
References provided by Crossref.org
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