Publication | Open Access
The GluR2 subunit inhibits proliferation by inactivating Src‐MAPK signalling and induces apoptosis by means of caspase 3/6‐dependent activation in glioma cells
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Citations
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References
2009
Year
ApoptosisCell DeathNeural Stem CellHigh-grade GliomasCancer BiologyGliomaTumor BiologyErk-src InactivationNeuro-oncologySignaling PathwayGlioblastoma MultiformeSrc‐mapk SignallingStem CellsRadiation OncologyCell SignalingCancer ResearchHealth SciencesGlioma CellsCell BiologyTumor MicroenvironmentScaffold Protein GripTumor SuppressorSystems BiologyMedicineGlioblastomaCaspase 3/6‐Dependent
Glioblastoma multiforme (GBM) is the most invasive and undifferentiated type of brain tumour, and so surgical interventions are ineffective. We found that GluR2 is absent in fast-growing GBM-derived tumour stem cells and high-grade glioma specimens, but is expressed in slow-growing stem cells and low-grade glioma specimens. More remarkably, GluR2 overexpression in U-87MG cells inhibits proliferation by inactivating extracellular signal-regulated kinase (ERK)1/2-Src phosphorylation and induces apoptosis. Mechanistically, we observed that the scaffold protein GRIP is essential for the effect of GluR2 on ERK-Src inactivation. These findings indicate that the absence of the GluR2 subunit favours malignancy.
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