JUN and glioblastoma: Patient-derived glioblastoma (BTSC168) cells treated with anisomycin increased phosphorylation of JNK, c-Jun and DNMT-1 expression levels and a significant increase in genome wide DNA methylation of promotor regions, whereas JNK inhibitor (SP600125, 50 μmol/mL) reduced protein levels of c-Jun, JNK and DNMT-1 with a reduction in global DNA methylation in CL3021 cells.