Aim: The aim of this study was to silence Ether à go-go 1 (EAG1) in glioma cells by RNAi in order to further analyze whether silencing this channel would improve injury caused by interferon gamma (IFN-γ).
Materials and methods: EAG1 silencing by the siRNAs EAG1hum_287 and EAG1hum_1727 (sequence targets 5'-GGCCTATTGTGTACAGCAATT-3' and 5'-GGGACTTCCTGAAGCTCTATT-3', respectively) was determined by reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability was measured by the 3-(4,5)-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide (MTT) assay. U-138MG glioma cells were injured by IFN-γ (25 ng/ml, 24 h) with or without the RNAi for EAG1 by a non-viral vector (pKV10.1-3, 0.2 μg).
Results: EAG1hum_287 and EAG1hum_1727 caused 0.46- and 0.52-fold decrease in EAG1 mRNA content, respectively. RNAi for EAG1 by pKv10.1-3 strengthened the reduction in cell viability caused by IFN-γ (11.4% versus 40.4%, p<0.05).
Conclusion: The present study reinforces the notion that EAG1 has a role in glioma biology, suggesting that this channel is a relevant player preserving the cell viability during IFN-γ injury.