Inhibition of epigenetic and cell cycle-related targets in glioblastoma cell lines: onametostat reduces proliferation and viability in both normoxic and hypoxic conditions

The objective of the study was to compare the transcriptome of the glioblastoma cell line T98-G following the 48-h treatment with 1 microM onametostat or 0.1% DMSO (negative control) under normoxic or hypoxic conditions. It was found that treatment with onametostat lead to dramatic changes in the transcriptome profile by inducing the cell cycle arrest, suppressing RNA splicing, and down-regulating several major glioblastoma cell survival pathways. The effect of hypoxia was less pronounced. Compare the expression of mRNAs in lysates of differently treated T98-G cells