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Hypoxia modulation of peroxisome proliferator‐activated receptors (PPARs) in human glioblastoma stem cells. Implications for therapy
Author(s) -
Galzio Renato,
Cristiano Loredana,
Fidoamore Alessia,
Cifone Maria Grazia,
Benedetti Elisabetta,
Cinque Benedetta,
Menghini Paola,
Raysi Dehcordi Sohelia,
Ippoliti Rodolfo,
Giordano Antonio,
Cimini Annamaria
Publication year - 2012
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24210
Subject(s) - peroxisome proliferator activated receptor , hypoxia (environmental) , stem cell , receptor , neural stem cell , cancer research , biology , stem cell therapy , radiation therapy , microbiology and biotechnology , pathology , endocrinology , medicine , chemistry , organic chemistry , oxygen
Abstract 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.