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http://hdl.handle.net/2445/33005
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DC Field | Value | Language |
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dc.contributor.author | Peña Rico, Miguel A. | - |
dc.contributor.author | Calvo-Vidal, María Nieves | - |
dc.contributor.author | Vilallonga Planells, Ruth | - |
dc.contributor.author | Martínez Soler, Fina | - |
dc.contributor.author | Giménez Bonafé, Pepita | - |
dc.contributor.author | Navarro i Sabaté, Àurea | - |
dc.contributor.author | Tortosa i Moreno, Avelina | - |
dc.contributor.author | Bartrons Bach, Ramon | - |
dc.contributor.author | Manzano Cuesta, Anna | - |
dc.date.accessioned | 2012-12-05T10:25:19Z | - |
dc.date.available | 2012-12-05T10:25:19Z | - |
dc.date.issued | 2011-11 | - |
dc.identifier.issn | 0167-8140 | - |
dc.identifier.uri | http://hdl.handle.net/2445/33005 | - |
dc.description.abstract | Background and purpose: The TP53 induced glycolysis and apoptosis regulator (TIGAR) functions to lower fructose-2,6-bisphosphate (Fru-2,6-P2) levels in cells, consequently decreasing glycolysis and leading to the scavenging of reactive oxygen species (ROS), which correlate with a higher resistance to cell death. The decrease in intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic lesions. Given these good prospects of TIGAR for metabolic regulation and p53-response modulation, we analyzed the effects of TIGAR knockdown in U87MG and T98G glioblastoma-derived cell lines. Methods/results: After TIGAR-knockdown in glioblastoma cell lines, different metabolic parameters were assayed, showing an increase in Fru-2,6-P2, lactate and ROS levels, with a concomitant decrease in reduced glutathione (GSH) levels. In addition, cell growth was inhibited without evidence of apoptotic or autophagic cell death. In contrast, a clear senescent phenotype was observed. We also found that TIGAR protein levels were increased shortly after irradiation. In addition, avoiding radiotherapy-triggered TIGAR induction by gene silencing resulted in the loss of capacity of glioblastoma cells to form colonies in culture and the delay of DNA repair mechanisms, based in c-H2AX foci, leading cells to undergo morphological changes compatible with a senescent phenotype. Thus, the results obtained raised the possibility to consider TIGAR as a therapeutic target to increase radiotherapy effects. Conclusion: TIGAR abrogation provides a novel adjunctive therapeutic strategy against glial tumors by increasing radiation-induced cell impairment, thus allowing the use of lower radiotherapeutic doses. | - |
dc.format.extent | 8 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Elsevier B.V. | - |
dc.relation.isformatof | Versió postprint del document publicat a: http://dx.doi.org/10.1016/j.radonc.2011.07.002 | - |
dc.relation.ispartof | Radiotherapy and Oncology, 2011, vol. 101, num. 1, p. 132-139 | - |
dc.relation.uri | http://dx.doi.org/10.1016/j.radonc.2011.07.002 | - |
dc.rights | (c) Elsevier B.V., 2011 | - |
dc.source | Articles publicats en revistes (Infermeria Fonamental i Clínica) | - |
dc.subject.classification | Glioma | - |
dc.subject.classification | Proteïnes supressores de tumors | - |
dc.subject.other | Gliomas | - |
dc.subject.other | Tumor suppressor protein | - |
dc.title | TP53 induced glycolysis and apoptosis regulator (TIGAR) knockdown results in radiosensitization of glioma cells | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/acceptedVersion | - |
dc.identifier.idgrec | 600411 | - |
dc.date.updated | 2012-12-05T10:25:19Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
Appears in Collections: | Articles publicats en revistes (Infermeria Fonamental i Clínica) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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File | Description | Size | Format | |
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600411.pdf | 893.24 kB | Adobe PDF | View/Open |
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