دورية أكاديمية
Hypoxia and succinate antagonize 2-deoxyglucose effects on glioblastoma
العنوان: | Hypoxia and succinate antagonize 2-deoxyglucose effects on glioblastoma |
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المؤلفون: | Pistollato F., Abbadi S., Rampazzo E., Viola G., Puppa A. D., Cavallini L., Frasson C., Persano L., Panchision D. M., Basso G. |
المساهمون: | Pistollato, F., Abbadi, S., Rampazzo, E., Viola, G., Puppa, A. D., Cavallini, L., Frasson, C., Persano, L., Panchision, D. M., Basso, G. |
سنة النشر: | 2010 |
المجموعة: | Padua Research Archive (IRIS - Università degli Studi di Padova) |
مصطلحات موضوعية: | 2-Deoxyglucose, GBM differentiation, Hypoxia, Hypoxia inducible factor-1α, Prolyl hydroxylase 2, Adult, Apoptosi, Blotting, Western, Cell Adhesion, Cell Culture Technique, Cell Differentiation, Cell Hypoxia, Cell Proliferation, Cell Survival, Cells, Cultured, Child, Deoxyglucose, Glutathione, Glycolysi, Human, Hypoxia-Inducible Factor 1, alpha Subunit, Immunohistochemistry, Membrane Potential, Mitochondrial, Oxygen, Reactive Oxygen Specie, Reverse Transcriptase Polymerase Chain Reaction |
الوصف: | Glioblastoma multiforme (GBM) are highly proliferative brain tumors characterized by a hypoxic microenvironment which controls GBM stem cell maintenance. Tumor hypoxia promotes also elevated glycolytic rate; thus, limiting glucose metabolism is a potential approach to inhibit tumor growth. Here we investigate the effects mediated by 2-deoxyglucose (2-DG), a glucose analogue, on primary GBM-derived cells maintained under hypoxia. Our results indicate that hypoxia protects GBM cells from the apoptotic effect elicited by 2-DG, which raises succinate dehydrogenase activity thus promoting succinate level decrease. As a consequence hypoxia inducible factor-1α (HIF-1α) degradation occurs and this induces GBM cells to acquire a neuronal committed phenotype. By adding succinate these effects are reverted, as succinate stabilizes HIF-1α and increases GBM stem cell fraction particularly under hypoxia, thus preserving the tumor stem cell niche.2-DG inhibits anaerobic glycolysis altering GBM cell phenotype by forcing tumor cells into mitochondrial metabolism and by inducing differentiation. © 2010 Elsevier Inc. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
العلاقة: | info:eu-repo/semantics/altIdentifier/pmid/20705058; info:eu-repo/semantics/altIdentifier/wos/WOS:000282850900007; volume:80; issue:10; firstpage:1517; lastpage:1527; numberofpages:11; journal:BIOCHEMICAL PHARMACOLOGY; http://hdl.handle.net/11577/3450250Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-77957016401 |
DOI: | 10.1016/j.bcp.2010.08.003 |
الإتاحة: | https://doi.org/10.1016/j.bcp.2010.08.003Test http://hdl.handle.net/11577/3450250Test |
رقم الانضمام: | edsbas.2E9154F2 |
قاعدة البيانات: | BASE |
DOI: | 10.1016/j.bcp.2010.08.003 |
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