596 Acta Neuropathol (2012) 123:587–600 Fig. 5 Treatment of medulloblastoma-bearing mice with PPARc antagonist GW9662 impairs glycolysis in tumor in vivo. a Western blot analysis for E2F1, PPARc, glycolysis (HKI, HKII, PKM2, and Glut4), lipid synthesis (FASN) and proliferation (cyclin D2) in samples of adjacent cerebella and medulloblastomas from vehicle (DMSO)- treated (-) or GW9662-treated (?) mice. The results shown are typical for several control and experimental sets of mice. b Immunostaining in adjacent cerebellum and medulloblastomas in vehicle- or GW9662- treated mice. Slides from the tissue of several untreated and treated NeuroD2-SmoA mice exhibiting medulloblastomas were analyzed and the presented results were typical. Magniﬁcation, 940. Bars 16 lM. c Effects of increasing doses of the PPARc antagonist GW9662 (0, 0.01, 0.02, 0.05, 0.07, 0.1 lM) for 24 h on pzp53med cell viability as determined by cell Titer-Glo assay, a bioluminescent analysis based on the presence of ATP. Each bar in the bioluminescence graph represents the average of separate quadruplicate determinations with error bars showing the standard deviation of the mean. Bars not sharing common letter are signiﬁcantly different at P \ 0.05 glycolysis and affect proliferation in these tumors. We treated medulloblastoma-bearing NeuroD2-SmoA1 mice with GW9662 or its vehicle DMSO for up to 10 days, then harvested the tumors for western blot and immunoﬂuorescence analysis. As shown in Fig. 5a, GW9662 treatment had no impact on the level of E2F1 or FASN, but sharply reduced PPARc protein levels (Fig. 5a, b), consistent with PPARc lying downstream of E2F1 and in a 123