The results demonstrated that the glioma neurosphere cells positively expressed stem cell marker SOX2, neuroectodermal stem cell marker Nestin, and also expressed astrocytes marker GFAP and neurons marker β-tubulin III fter FBS-induced differentiation for a week, which proved the glioma neurosphere cells have the self-renewal and multipotential differentiation capacity.
We also observed co-expression of Sox2 and GFAP, another suggested marker of glioma cancer stem cells, indicating that the putative cancer stem cells in GBM9 tumors expressed both of these markers.
Immunohistochemical analyses demonstrated a diffusely GFAP-positive glial neoplasm with mixed populations of cells that were variably positive for Olig2, NHERF1, Sox2, and CD44.
These cases seem to represent an unusual primarily extra-axial presentation of pleomorphic xanthoastrocytoma and may account for at least some of the previously reported cases of primary meningeal glioma and/or glial fibrillary acidic protein-immunoreactive meningioma variants.
We found that Nestin (a type VI intermediate filament protein), like the glioma stem cell (GSC) markers CD133 and CD15, exhibited different levels of expression in primary human glioblastoma specimens.
Implanted mouse and human glioma- but not fibroblast-containing HF attracted microglia and up-regulated immunoreactivity for GFAP, which is a marker of astrogliosis.
Intriguingly, Sema5A induces re-expression of glial fibrillary acidic protein (GFAP), which when silenced restricts differentiation of glioma cells to bipolar instead of multipolar morphology.
Double transgenic GFAP-Cre/Rictor(loxP/loxP) mice developed multifocal infiltrating glioma containing elevated mTORC2 activity and typically involved the subventricular zone (SVZ) and lateral ventricle.
Our results suggest that epigenetic silencing of the GFAP gene through DNA methylation of its promoter region may be one mechanism by which GFAP is downregulated in human gliomas and glioma cell lines.
Overexpression of NFI-X3 dramatically up-regulates GFAP and SPARCL1 expression in glioma cells, whereas the knockdown of NFI-X3 diminishes the expression of both GFAP and SPARCL1 in astrocytes.
Our result suggests that glioma consists of at least two different cell populations: Sox2(+) /GFAP(+) /Sox21(+) /FN(-) and Sox2(-) /GFAP(-) /Sox21(-) /FN(+) .
It promoted p53-dependent morphological differentiation of U343MGa Cl2:6 glioma cells as evidenced by intensified expression of glial fibrillary acidic protein and profound changes in cell shape.
Immunocytochemical analysis, using an antibody against Delta164 and Deltaexon6 (GFAP+1), was performed in surgical specimens of patients with hippocampal sclerosis (HS), focal cortical dysplasia type IIB (FCD), cortical tubers of tuberous sclerosis complex (TSC), glioneuronal and glial tumors.
Results of staining with glial fibrillary acidic protein were not consistent with a glioma, and staining with INI-1 was inconsistent with atypical teratoid/rhabdoid tumor.
Other promising biomarkers in glioma research include glial fibrillary acidic protein, galectins, Kir potassium channel proteins, angiogenesis, and apoptosis pathway markers.
As a feasibility study, we isolated a C6 rat glioma cell line stably transfected with a lacZ reporter gene driven by the gfa2 human GFAP promoter fragment.