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Hypoxia modulation of peroxisome proliferator-activated receptors (PPARs) in human glioblastoma stem cells. Implications for therapy
Journal of cellular biochemistry, 2012-11, Vol.113 (11), p.3342-3352
Galzio, Renato
Cristiano, Loredana
Fidoamore, Alessia
Cifone, Maria Grazia
Benedetti, Elisabetta
Cinque, Benedetta
Menghini, Paola
Raysi Dehcordi, Sohelia
Ippoliti, Rodolfo
Giordano, Antonio
Cimini, Annamaria
2012
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Galzio, Renato
Cristiano, Loredana
Fidoamore, Alessia
Cifone, Maria Grazia
Benedetti, Elisabetta
Cinque, Benedetta
Menghini, Paola
Raysi Dehcordi, Sohelia
Ippoliti, Rodolfo
Giordano, Antonio
Cimini, Annamaria
Titel
Hypoxia modulation of peroxisome proliferator-activated receptors (PPARs) in human glioblastoma stem cells. Implications for therapy
Ist Teil von
Journal of cellular biochemistry, 2012-11, Vol.113 (11), p.3342-3352
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2012
Quelle
MEDLINE
Beschreibungen/Notizen
Gliobastoma (GB), the most common adult brain tumor, infiltrates normal brain area rendering impossible the complete surgical resection, resulting in a poor median survival (14–15 months), despite the aggressive multimodality treatments post‐surgery, such as radiation and chemo‐therapy. GB is characterized by hypoxic and necrotic regions due to a poorly organized tumor vascularization, leading to inadequate blood supply and consequently to hypoxic and necrotic areas. We have previously shown that, under hypoxia GB primary cells increased the expression of stemness markers as well as the expression of the nuclear receptor peroxisome proliferator‐activated receptor α (PPARα) and also the crucial role played by PPARs in mouse neural stem cells maintenance and differentiation. Due to the importance of lipid signaling in cell proliferation and differentiation, in this work, we analyzed the expression of PPARs in GB neurospheres both in normoxic and hypoxic conditions. The results obtained suggest a differential regulation of the three PPARs by hypoxia, thus indicating a possible therapeutic strategy to counteract GB recurrencies. J. Cell. Biochem. 113: 3342–3352, 2012. © 2012 Wiley Periodicals, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0730-2312
eISSN: 1097-4644
DOI: 10.1002/jcb.24210
Titel-ID: cdi_proquest_miscellaneous_1439221074
Format
–
Schlagworte
Biomarkers - metabolism
,
Blotting, Western
,
Brain Neoplasms - genetics
,
Brain Neoplasms - metabolism
,
Brain Neoplasms - pathology
,
Cell Hypoxia
,
Cell Line, Tumor
,
Cell Proliferation - drug effects
,
Cholesterol - metabolism
,
Gene Expression Regulation, Neoplastic - drug effects
,
Glioblastoma - genetics
,
Glioblastoma - metabolism
,
Glioblastoma - pathology
,
GLIOBLASTOMA STEM CELLS
,
Humans
,
HYPOXIA
,
Microscopy, Fluorescence
,
Neoplastic Stem Cells - drug effects
,
Neoplastic Stem Cells - metabolism
,
Neoplastic Stem Cells - pathology
,
Oxygen - pharmacology
,
PPAR alpha - genetics
,
PPAR alpha - metabolism
,
PPAR gamma - genetics
,
PPAR gamma - metabolism
,
PPAR-beta - genetics
,
PPAR-beta - metabolism
,
PPARs
,
Signal Transduction
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