دورية أكاديمية
أعرض في EDS

FOXM1 repression increases mitotic death upon antimitotic chemotherapy through BMF upregulation.

التفاصيل البيبلوغرافية
العنوان: FOXM1 repression increases mitotic death upon antimitotic chemotherapy through BMF upregulation.
المؤلفون: Vaz S; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135, Porto, Portugal.; Aging and Aneuploidy Group, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135, Porto, Portugal.; Programa doutoral em Biologia Molecular e Celular, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4050-313, Porto, Portugal., Ferreira FJ; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135, Porto, Portugal.; Aging and Aneuploidy Group, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135, Porto, Portugal.; Vertebrate Development and Regeneration Group, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135, Porto, Portugal.; Graduate Program in Areas of Basic and Applied Biology (GABBA), Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Universidade do Porto, 4050-313, Porto, Portugal., Macedo JC; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135, Porto, Portugal.; Aging and Aneuploidy Group, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135, Porto, Portugal., Leor G; Department of Human Molecular Genetics & Biochemistry, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel., Ben-David U; Department of Human Molecular Genetics & Biochemistry, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel., Bessa J; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135, Porto, Portugal.; Vertebrate Development and Regeneration Group, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135, Porto, Portugal., Logarinho E; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135, Porto, Portugal. elsa.logarinho@ibmc.up.pt.; Aging and Aneuploidy Group, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135, Porto, Portugal. elsa.logarinho@ibmc.up.pt.
المصدر: Cell death & disease [Cell Death Dis] 2021 May 25; Vol. 12 (6), pp. 542. Date of Electronic Publication: 2021 May 25.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101524092 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-4889 (Electronic) NLM ISO Abbreviation: Cell Death Dis Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Pub. Group
مواضيع طبية MeSH: Cell Death*/drug effects , Cell Death*/genetics, Antimitotic Agents/*pharmacology , Forkhead Box Protein M1/*genetics, Adaptor Proteins, Signal Transducing/genetics ; Aged, 80 and over ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Apoptosis/genetics ; Cells, Cultured ; Child ; Down-Regulation/genetics ; Fibroblasts/drug effects ; Fibroblasts/physiology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MCF-7 Cells ; Male ; Mitosis/drug effects ; Mitosis/genetics ; Up-Regulation/drug effects ; Up-Regulation/genetics
مستخلص: Inhibition of spindle microtubule (MT) dynamics has been effectively used in cancer treatment. Although the mechanisms by which MT poisons elicit mitotic arrest are fairly understood, efforts are still needed towards elucidating how cancer cells respond to antimitotic drugs owing to cytotoxicity and resistance side effects. Here, we identified the critical G2/M transcription factor Forkhead box M1 (FOXM1) as a molecular determinant of cell response to antimitotics. We found FOXM1 repression to increase death in mitosis (DiM) due to upregulation of the BCL-2 modifying factor (BMF) gene involved in anoikis, an apoptotic process induced upon cell detachment from the extracellular matrix. FOXM1 binds to a BMF intronic cis-regulatory element that interacts with both the BMF and the neighbor gene BUB1B promoter regions, to oppositely regulate their expression. This mechanism ensures that cells treated with antimitotics repress BMF and avoid DiM when FOXM1 levels are high. In addition, we show that this mechanism is partly disrupted in anoikis/antimitotics-resistant tumor cells, with resistance correlating with lower BMF expression but in a FOXM1-independent manner. These findings provide a stratification biomarker for antimitotic chemotherapy response.
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المشرفين على المادة: 0 (Adaptor Proteins, Signal Transducing)
0 (Antimitotic Agents)
0 (Antineoplastic Agents)
0 (BMF protein, human)
0 (FOXM1 protein, human)
0 (Forkhead Box Protein M1)
تواريخ الأحداث: Date Created: 20210526 Date Completed: 20210922 Latest Revision: 20210922
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8149823
DOI: 10.1038/s41419-021-03822-5
PMID: 34035233
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-4889
DOI:10.1038/s41419-021-03822-5