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Mitochondrial fragmentation, elevated mitochondrial superoxide and respiratory supercomplexes disassembly is connected with the tamoxifen-resistant phenotype of breast cancer cells

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    SYSNO ASEP0520490
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleMitochondrial fragmentation, elevated mitochondrial superoxide and respiratory supercomplexes disassembly is connected with the tamoxifen-resistant phenotype of breast cancer cells
    Author(s) Tomkova, Veronika (BTO-N)
    Sandoval-Acuna, Cristian (BTO-N)
    Torrealba, Natalia (BTO-N)
    Truksa, Jaroslav (BTO-N) RID, ORCID
    Number of authors4
    Source TitleFree Radical Biology and Medicine. - : Elsevier - ISSN 0891-5849
    Roč. 143, NOV 1 2019 (2019), s. 510-521
    Number of pages12 s.
    Languageeng - English
    CountryUS - United States
    Keywordsactivated protein-kinase ; estrogen-receptor-alpha ; acquired-resistance ; Mitochondrial fragmentation ; Reactive oxygen species
    Subject RIVEB - Genetics ; Molecular Biology
    OECD categoryBiochemistry and molecular biology
    R&D ProjectsGA16-12816S GA ČR - Czech Science Foundation (CSF)
    GA18-13103S GA ČR - Czech Science Foundation (CSF)
    ED1.1.00/02.0109 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    LQ1604 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Method of publishingOpen access
    Institutional supportBTO-N - RVO:86652036
    UT WOS000496132900047
    DOI10.1016/j.freeradbiomed.2019.09.004
    AnnotationTamoxifen resistance remains a clinical obstacle in the treatment of hormone sensitive breast cancer. It has been reported that tamoxifen is able to target respiratory complex I within mitochondria. Therefore, we established two tamoxifen-resistant cell lines, MCF7 Tam5R and T47D Tam5R resistant to 5 mu M tamoxifen and investigated whether tamoxifen-resistant cells exhibit mitochondrial changes which could help them survive the treatment. The function of mitochondria in this experimental model was evaluated in detail by studying i) the composition and activity of mitochondrial respiratory complexes, ii) respiration and glycolytic status, iii) mitochondrial distribution, dynamics and reactive oxygen species production. We show that Tam5R cells exhibit a significant decrease in mitochondrial respiration, low abundance of assembled mitochondrial respiratory supercomplexes, a more fragmented mitochondrial network connected with DRP1 Ser637 phosphorylation, higher glycolysis and sensitivity to 2-deoxyglucose. Tam5R cells also produce significantly higher levels of mitochondrial superoxide but at the same time increase their antioxidant defense (CAT, SOD2) through upregulation of SIRT3 and show phosphorylation of AMPK at Ser 485/491. Importantly, MCF7 rho 0 cells lacking functional mitochondria exhibit a markedly higher resistance to tamoxifen, supporting the role of mitochondria in tamoxifen resistance. We propose that reduced mitochondrial function and higher level of reactive oxygen species within mitochondria in concert with metabolic adaptations contribute to the phenotype of tamoxifen resistance.
    WorkplaceInstitute of Biotechnology
    ContactMonika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700
    Year of Publishing2020
    Electronic addresshttps://www.sciencedirect.com/science/article/pii/S0891584919310044?via%3Dihub
Number of the records: 1  

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