Open AccessSOX2 Silencing in Glioblastoma Tumor‐Initiating Cells Causes Stop of Proliferation and Loss of Tumorigenicity
Author(s) -
Gangemi Rosaria Maria Rita,
Griffero Fabrizio,
Marubbi Daniela,
Perera Marzia,
Capra Maria Cristina,
Malatesta Paolo,
Ravetti Gian Luigi,
Zona Gian Luigi,
Daga Antonio,
Corte Giorgio
Publication year - 2009
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1634/stemcells.2008-0493
Subject(s) - sox2 , biology , glioblastoma , neural stem cell , stem cell , cancer research , gene silencing , neurosphere , cancer stem cell , gene , immunology , microbiology and biotechnology , cellular differentiation , adult stem cell , genetics , embryonic stem cell
Glioblastoma, the most aggressive cerebral tumor, is invariably lethal. Glioblastoma cells express several genes typical of normal neural stem cells. One of them, SOX2 , is a master gene involved in sustaining self‐renewal of several stem cells, in particular neural stem cells. To investigate its role in the aberrant growth of glioblastoma, we silenced SOX2 in freshly derived glioblastoma tumor‐initiating cells (TICs). Our results indicate that SOX2 silenced glioblastoma TICs, despite the many mutations they have accumulated, stop proliferating and lose tumorigenicity in immunodeficient mice. SOX2 is then also fundamental for maintenance of the self‐renewal capacity of neural stem cells when they have acquired cancer properties. SOX2, or its immediate downstream effectors, would then be an ideal target for glioblastoma therapy. S TEM C ELLS 2009;27:40–48