Cell Cycle Changes after Glioblastoma Stem Cell Irradiation: The Major Role of RAD51

Autor: Gaëlle Tachon, Pierre Rivet, Odile Boissonnade, Pierre-Olivier Guichet, Konstantin Masliantsev, Antoine Berger, Michel Wager, Lucie Karayan-Tapon, Ulrich Cortes, Anais Balbous
Přispěvatelé: Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Institut National de la Transfusion Sanguine [Paris] (INTS), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de neurosciences expérimentales et cliniques (LNEC), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire Cancérologie Biologique Poitiers, Laboratoire d'Immunologie et Immunopathologie [CHU Poitiers] (CNRS URA 1172), Centre hospitalier universitaire de Poitiers (CHU Poitiers)-Centre National de la Recherche Scientifique (CNRS), Institut des Neurosciences de Montpellier - Déficits sensoriels et moteurs (INM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Laboratoire de Physique et Physiologie Intégratives de l'Arbre Fruitier et Forestier (PIAF), Institut National de la Recherche Agronomique (INRA)-Université Blaise Pascal - Clermont-Ferrand 2 (UBP), Institut Sophia Agrobiotech [Sophia Antipolis] (ISA), Institut National de la Recherche Agronomique (INRA)-Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Cellules souches leucémiques et thérapeuthiques, Université de Poitiers-Centre hospitalier universitaire de Poitiers (CHU Poitiers)
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
endocrine system
Cell cycle checkpoint
DNA Repair
DNA damage
RAD51
[SDV.CAN]Life Sciences [q-bio]/Cancer
Glioma Stem Cells
Biology
Radiation Tolerance
Catalysis
Article
Inorganic Chemistry
lcsh:Chemistry
03 medical and health sciences
0302 clinical medicine
Glioma
Radioresistance
Cell Line
Tumor
Radiation
Ionizing
medicine
Humans
Physical and Theoretical Chemistry
Molecular Biology
lcsh:QH301-705.5
Spectroscopy
ComputingMilieux_MISCELLANEOUS
Organic Chemistry
fungi
General Medicine
Cell cycle
Cell sorting
medicine.disease
Computer Science Applications
Gene Expression Regulation
Neoplastic
DNA repair protein RAD51 homolog 1 (RAD51)
030104 developmental biology
lcsh:Biology (General)
lcsh:QD1-999
030220 oncology & carcinogenesis
Cancer research
Neoplastic Stem Cells
cell cycle
Rad51 Recombinase
Stem cell
Glioblastoma
ionizing radiation
Zdroj: International Journal of Molecular Sciences
Volume 19
Issue 10
International Journal of Molecular Sciences, MDPI, 2018, 19 (10), pp.3018. ⟨10.3390/ijms19103018⟩
International Journal of Molecular Sciences, Vol 19, Iss 10, p 3018 (2018)
ISSN: 1422-0067
1661-6596
DOI: 10.3390/ijms19103018
Popis: &ldquo
Glioma Stem Cells&rdquo
(GSCs) are known to play a role in glioblastoma (GBM) recurrence. Homologous recombination (HR) defects and cell cycle checkpoint abnormalities can contribute concurrently to the radioresistance of GSCs. DNA repair protein RAD51 homolog 1 (RAD51) is a crucial protein for HR and its inhibition has been shown to sensitize GSCs to irradiation. The aim of this study was to examine the consequences of ionizing radiation (IR) for cell cycle progression in GSCs. In addition, we intended to assess the potential effect of RAD51 inhibition on cell cycle progression. Five radiosensitive GSC lines and five GSC lines that were previously characterized as radioresistant were exposed to 4Gy IR, and cell cycle analysis was done by fluorescence-activated cell sorting (FACS) at 24, 48, 72, and 96 h with or without RAD51 inhibitor. Following 4Gy IR, all GSC lines presented a significant increase in G2 phase at 24 h, which was maintained over 72 h. In the presence of RAD51 inhibitor, radioresistant GSCs showed delayed G2 arrest post-irradiation for up to 48 h. This study demonstrates that all GSCs can promote G2 arrest in response to radiation-induced DNA damage. However, following RAD51 inhibition, the cell cycle checkpoint response differed. This study contributes to the characterization of the radioresistance mechanisms of GSCs, thereby supporting the rationale of targeting RAD51-dependent repair pathways in view of radiosensitizing GSCs.
Databáze: OpenAIRE
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