Fig. 5

Characteristic mutations for lower/high grade gliomas exert no overt effect on PTP expression patterns. a Immunoblot of lysates from U-251 MG glioblastoma cells expressing wild-type EGFR, EGFRvIII or empty vector (EV) control. Cells were treated with the EGFR inhibitor Gefitinib (or DMSO as solvent control) for 48 h before being lysed. Immunostaining (IB) was with antibodies against EGFR, phosphotyrosine (pY) or GAPDH (as loading control). b Immunoblot analysis for PTEN and Ser473-phosphorylated AKT levels in parental and (PTEN-targeted) CRISPR/Cas9-treated LN-229 cells. Lysates were prepared following 8 h of serum starvation (0.5 % FCS), and tubulin immunostaining served as loading control. c-e Analysis of (ACTB-normalized) DUSP16, PTPRG and PTPRT transcript levels, as determined by qPCR, in cell models mimicking EGFR hyperactivity (c), PTEN deficiency (d) or mutant IDH1-mediated 2-HG exposure (e). Bars indicate mean with SEM, asterisk represents significance level (* p < 0.05)