Pharmacological blockade of mGlu2/3 metabotropic glutamate receptors reduces cell proliferation in cultured human glioma cells.

摘要: Glial cell proliferation in culture is under the control of metabotropic glutamate (mGlu) receptors. We have examined whether this extends to human glioma cells. Primary cultures were prepared from surgically removed glioblastomas. RT-PCR combined with western blot analysis showed that most (eight out 11) expressed group-II mGlu In two selected (MZC-12 and FCN-9), mGlu2/3 receptor antagonist, LY341495, slowed when applied growth medium second day after plating. This effect was reversible because linear restored washing drug. LY341495 reduced at concentrations lower than 100 nM, which are considered as selective for addition, its action mimicked by putative antagonist (2S)-a-ethylglutamate. The anti-proliferative confirmed measuring [methyl- 3 H]-thymidine incorporation arrested G0 phase cycle then stimulated proliferate addition 10% fetal calf serum or ng/mL epidermal factor (EGF). treated EGF, also able reduce stimulation mitogen-activated protein kinase (MAPK) pathway, well induction cyclin D1. Both effects, decreased incorporation, partially co-addition potent agonist, LY379268. conclude activation receptors supports cells antagonists these should be tested their ability tumour vivo.