ArticleRadiation oncology (London, England)2011
Delayed cell death associated with mitotic catastrophe in γ-irradiated stem-like glioma cells.
Article in Radiation oncology (London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 39 citations in OpenAlex.
- From survival of irradiated mice to modern molecular insights: a seventy-year journey in radiobiology at the institute of biophysics, Czech academy of sciences.European biophysics journal : EBJ · 2025Review
- The temporal response of a glioma cell population to irradiation: modelling the effect of dose and cell density.Royal Society open science · 2025Article
- Alterations in Molecular Profiles Affecting Glioblastoma Resistance to Radiochemotherapy: Where Does the Good Go?Cancers · 2022Review
- MicroRNA-107 enhances radiosensitivity by suppressing granulin in PC-3 prostate cancer cells.Scientific reports · 2020Article
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- Impaired Notch Signaling Leads to a Decrease in p53 Activity and Mitotic Catastrophe in Aged Muscle Stem Cells.Cell stem cell · 2018Article
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- mRNA and methylation profiling of radioresistant esophageal cancer cells: the involvement of Sall2 in acquired aggressive phenotypes.Journal of Cancer · 2017Article
- Nitric oxide released from JS-K induces cell death by mitotic catastrophe as part of necrosis in glioblastoma multiforme.Cell death & disease · 2016Article
- FoxO proteins or loss of functional p53 maintain stemness of glioblastoma stem cells and survival after ionizing radiation plus PI3K/mTOR inhibition.Oncotarget · 2016Article
- Silencing erythropoietin receptor on glioma cells reinforces efficacy of temozolomide and X-rays through senescence and mitotic catastrophe.Oncotarget · 2015Article
- Patient-derived glioblastoma stem cells are killed by CD133-specific CAR T cells but induce the T cell aging marker CD57.Oncotarget · 2015Article
- Current concepts in clinical radiation oncology.Radiation and environmental biophysics · 2014Review
- The failure in the stabilization of glioblastoma-derived cell lines: spontaneous in vitro senescence as the main culprit.PloS one · 2014Article
- Ionizing radiation in glioblastoma initiating cells.Frontiers in oncology · 2013Article
- uPAR and cathepsin B inhibition enhanced radiation-induced apoptosis in gliomainitiating cells.Neuro-oncology · 2012Article
- Article
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6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeStem-like tumor cells are regarded as highly resistant to ionizing radiation (IR). Previous studies have focused on apoptosis early after irradiation, and the apoptosis resistance observed has been attributed to reduced DNA damage or enhanced DNA repair compared to non-stem tumor cells. Here, early and late radioresponse of patient-derived stem-like glioma cells (SLGCs) and differentiated cells directly derived from them were examined for cell death mode and the influence of stem cell-specific growth factors. MATERIALS AND
methodsPrimary SLGCs were propagated in serum-free medium with the stem-cell mitogens epidermal growth factor (EGF) and fibroblast growth factor-2 (FGF-2). Differentiation was induced by serum-containing medium without EGF and FGF. Radiation sensitivity was evaluated by assessing proliferation, clonogenic survival, apoptosis, and mitotic catastrophe. DNA damage-associated γH2AX as well as p53 and p21 expression were determined by Western blots.
resultsSLGCs failed to apoptose in the first 4 days after irradiation even at high single doses up to 10 Gy, but we observed substantial cell death later than 4 days postirradiation in 3 of 6 SLGC lines treated with 5 or 10 Gy. This delayed cell death was observed in 3 of the 4 SLGC lines with nonfunctional p53, was associated with mitotic catastrophe and occurred via apoptosis. The early apoptosis resistance of the SLGCs was associated with lower γH2AX compared to differentiated cells, but we found that the stem-cell culture cytokines EGF plus FGF-2 strongly reduce γH2AX levels. Nonetheless, in two p53-deficient SLGC lines examined γIR-induced apoptosis even correlated with EGF/FGF-induced proliferation and mitotic catastrophe. In a line containing CD133-positive and -negative stem-like cells, the CD133-positive cells proliferated faster and underwent more γIR-induced mitotic catastrophe.
conclusionsOur results suggest the importance of delayed apoptosis, associated mitotic catastrophe, and cellular proliferation for γIR-induced death of p53-deficient SLGCs. This may have therapeutic implications. We further show that the stem-cell culture cytokines EGF plus FGF-2 activate DNA repair and thus confound in vitro comparisons of DNA damage repair between stem-like and more differentiated tumor cells.
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