ArticleRadiation oncology (London, England)2011
Radioresistance of human glioma spheroids and expression of HSP70, p53 and EGFr.
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 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
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- Targeted Profiling of Heat Shock Proteome in Radioresistant Breast Cancer Cells.Chemical research in toxicology · 2019Article
- Modeling of the metabolic energy dissipation for restricted tumor growth.Journal of bioenergetics and biomembranes · 2017Article
- Modeling tumor cell adaptations to hypoxia in multicellular tumor spheroids.Journal of experimental & clinical cancer research : CR · 2017Review
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- Progression inference for somatic mutations in cancer.Heliyon · 2017Article
- Deubiquitylating enzyme USP9x regulates radiosensitivity in glioblastoma cells by Mcl-1-dependent and -independent mechanisms.Cell death & disease · 2016Article
- Increasing radiosensitivity with the downregulation of cofilin-1 in U251 human glioma cells.Molecular medicine reports · 2015Article
- Targeting of EGFR and HER2 with therapeutic antibodies and siRNA: a comparative study in glioblastoma cells.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2015Article
- LRIG1 enhances the radiosensitivity of radioresistant human glioblastoma U251 cells via attenuation of the EGFR/Akt signaling pathway.International journal of clinical and experimental pathology · 2015Article
- Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRadiation therapy is routinely prescribed for high-grade malignant gliomas. However, the efficacy of this therapeutic modality is often limited by the occurrence of radioresistance, reflected as a diminished susceptibility of the irradiated cells to undergo cell death. Thus, cells have evolved an elegant system in response to ionizing radiation induced DNA damage, where p53, Hsp70 and/or EGFr may play an important role in the process. In the present study, we investigated whether the content of p53, Hsp70 and EGFr are associated to glioblastoma (GBM) cell radioresistance.
methodsSpheroids from U-87MG and MO59J cell lines as well as spheroids derived from primary culture of tumor tissue of one GBM patient (UGBM1) were irradiated (5, 10 and 20 Gy), their relative radioresistance were established and the p53, Hsp70 and EGFr contents were immunohistochemically determined. Moreover, we investigated whether EGFr-phospho-Akt and EGFr-MEK-ERK pathways can induce GBM radioresistance using inhibitors of activation of ERK (PD098059) and Akt (wortmannin).
resultsAt 5 Gy irradiation UGBM1 and U-87MG spheroids showed growth inhibition whereas the MO59J spheroid was relatively radioresistant. Overall, no significant changes in p53 and Hsp70 expression were found following 5 Gy irradiation treatment in all spheroids studied. The only difference observed in Hsp70 content was the periphery distribution in MO59J spheroids. However, 5 Gy treatment induced a significant increase on the EGFr levels in MO59J spheroids. Furthermore, treatment with inhibitors of activation of ERK (PD098059) and Akt (wortmannin) leads to radiosensitization of MO59J spheroids.
conclusionsThese results indicate that the PI3K-Akt and MEK-ERK pathways triggered by EGFr confer GBM radioresistance.
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