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    Título
    Chloroquine-induced DNA damage synergizes with DNA repair inhibitors causing cancer cell death
    Autor(es)
    Iglesias Corral, Diego
    García Vallés, Paula
    Arroyo Garrapucho, Nuria
    Bueno Martínez, Elena
    Ruiz Robles, Juan Manuel
    Ovejero-Sánchez, María
    González Sarmiento, RogelioAutoridad USAL
    Herrero Hernández, Ana Belén
    Palabras clave
    Cloroquine
    DNA damage
    DNA repair
    Cancer
    Cell line
    Fecha de publicación
    2024
    Editor
    FRONTIERS
    Citación
    Iglesias-Corral, D., García-Valles, P., Arroyo-Garrapucho, N., Bueno-Martínez, E., Ruiz-Robles, J. M., Ovejero-Sánchez, M., González-Sarmiento, R., & Herrero, A. B. (2024). Chloroquine-induced DNA damage synergizes with DNA repair inhibitors causing cancer cell death. Frontiers in Oncology, 14. https://doi.org/10.3389/FONC.2024.1390518
    Resumen
    [EN]Cancer is a global health problem accounting for nearly one in six deaths worldwide. Conventional treatments together with new therapies have increased survival to this devastating disease. However, the persistent challenges of treatment resistance and the limited therapeutic arsenal available for specific cancer types still make research in new therapeutic strategies an urgent need. Chloroquine was tested in combination with different drugs (Panobinostat, KU-57788 and NU-7026) in 8 human-derived cancer cells lines (colorectal: HCT116 and HT29; breast: MDA-MB-231 and HCC1937; glioblastoma: A-172 and LN-18; head and neck: CAL-33 and 32816). Drug´s effect on proliferation was tested by MTT assays and cell death was assessed by Anexin V-PI apoptosis assays. The presence of DNA double-strand breaks was analyzed by phospho-H2AX fluorescent staining. To measure homologous recombination efficiency the HR-GFP reporter was used, which allows flow cytometry-based detection of HR stimulated by I-SceI endonuclease-induced DSBs. The combination of chloroquine with any of the drugs employed displayed potent synergistic effects on apoptosis induction, with particularly pronounced efficacy observed in glioblastoma and head and neck cancer cell lines. We found that chloroquine produced DNA double strand breaks that depended on reactive oxygen species formation, whereas Panobinostat inhibited DNA double-strand breaks repair by homologous recombination. Cell death caused by chloroquine/Panobinostat combination were significantly reduced by N-Acetylcysteine, a reactive oxygen species scavenger, underscoring the pivotal role of DSB generation in CQ/LBH-induced lethality. Based on these data, we also explored the combination of CQ with KU-57788 and NU-7026, two inhibitors of the other main DSB repair pathway, nonhomologous end joining (NHEJ), and again synergistic effects on apoptosis induction were observed. Our data provide a rationale for the clinical investigation of CQ in combination with DSB inhibitors for the treatment of different solid tumors.
    URI
    http://hdl.handle.net/10366/164476
    ISSN
    2234-943X
    DOI
    10.3389/fonc.2024.1390518
    Versión del editor
    https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2024.1390518/full
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    2024 © UNIVERSIDAD DE SALAMANCA