Abstract
Objective To discuss the effects of metabotropic glutamate receptor 5 subtype (mGluR5) on proliferation of U251 cells and the underlying mechanism by observing the effect of antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) on proliferation of U251 cells.Methods Human glioma cell line U251 was conventionally cultured in vitro; MTT assay was employed to detect the effects of 100 μmol/L MPEP,20 μmol/L SP600125 (antagonist to JNK) and 400 multiplicity of infection (MOI) adenoviruses-△169 (negatively dominant virus ofc-Jun) for 48 h on U251 cells.Western blotting was used to observe the expressions of phosphorylated c-Jun and phosphorylated JNK in U251 cells after being treated with different concentrations of MPEP (5,10,20,50 and 100 μmol/L) for 24 h andwith 100 μmol/LMPEP for4,8,12and24h.Results MTT assay showed that U251 cellsbeing treated with 100 μmol/L MPEP,20 μmoUL SP600125 and 400MOI Ad-△169 for 48 h had significantly lower absorbance value than their control groups (P＜0.05).Western blotting indicated that the expressions of phosphorylated c-Jun and phosphorylated JNK in U251 cells being treated with 5,10,20,50 and 100 μmol/L MPEP for 24 h were significantly lower than those in normal controls (P＜0.05); the higher the MPEP concentration,the lower the expression ofphosphorylated c-Jun.The expressions of phosphorylated c-Jun and phosphorylated JNK in U251 cells being treated with 100 μmol/L MPEP for 4,8,12 and 24 h were significantly lower than those in normal controls (P＜0.05); the longer the MPEP given time,the lower the expression ofphosphorylated c-Jun.Conclusions MPEP,the antagonist mGluR5,could significantly promote cell proliferation of U251,which might be relevant to the expressions of phosphorylated c-Jun and phosphorylated JNK in JNK pathway,and the trend is concentration-dependent and time-dependent. Key words: Glioma; U251 cell; Metabotropic glutamate receptor 5 subtype; Proliferation
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