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Forced expression of Sox21 inhibits Sox2 and induces apoptosis in human glioma cells
Author(s) -
Ferletta Maria,
Caglayan Demet,
Mokvist Liza,
Jiang Yiwen,
Kastemar Marianne,
Uhrbom Lene,
Westermark Bengt
Publication year - 2010
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.25647
Subject(s) - sox2 , biology , glioma , microbiology and biotechnology , progenitor cell , ectopic expression , cancer research , cell culture , stem cell , gene , genetics , embryonic stem cell
Numerous studies support a role for Sox2 to keep stem cells and progenitor cells in an immature and proliferative state. Coexpression of Sox2 and GFAP has been found in regions of the adult brain where neural stem cells are present and in human glioma cells. In our study, we have investigated the roles of Sox2 and its counteracting partner Sox21 in human glioma cells. We show for the first time that Sox21 is expressed in both primary glioblastoma and in human glioma cell lines. We found that coexpression of Sox2, GFAP and Sox21 was mutually exclusive with expression of fibronectin. Our result suggests that glioma consists of at least two different cell populations: Sox2 + /GFAP + /Sox21 + /FN − and Sox2 − /GFAP − /Sox21 − /FN + . Reduction of Sox2 expression by using siRNA against Sox2 or by overexpressing Sox21 using a tetracycline‐regulated expression system (Tet‐on) caused decreased GFAP expression and a reduction in cell number due to induction of apoptosis. We suggest that Sox21 can negatively regulate Sox2 in glioma. Our findings imply that Sox2 and Sox21 may be interesting targets for the development of novel glioma therapy.