Skip to main content
. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Clin Cancer Res. 2016 Aug 19;23(5):1250–1262. doi: 10.1158/1078-0432.CCR-15-2888

Figure 4. Treatment of NRAS/LgT derived GBM cells with AMD3100 (Plerixafor).

Figure 4

A. Western blot analysis of M7 (NRAS/LgT) cells probing with antibodies against retinoblastoma (Rb and phospho-RbS807/811), pAkt, Bcl-XL and Cyclin D1 during a 5 day time-course of AMD3100 treatment. Lanes represent duplicate treatment flasks with (+) or without (-) AMD3100. β-actin was used as a loading control. B. QPCR analysis of gene expression in cells treated or not with AMD3100, during a 5 day time-course, to analyze expression of cyclin D1, cdk4 and cdk6, cxcl12, hif1-α and tgf-β represented graphically as relative expression compared to hprt. Error bars represent SEM of triplicate treatment wells. C. Cell proliferation analysis of M7 (NRAS/LgT) cells treated or not with AMD3100 (10µM) and CXCL12 (20nM) showing that exogenous CXCL12 rescues the AMD3100 decrease in proliferation, but does not increase proliferation in the absence of AMD3100 Statistical test: two-way ANOVA with Boferronni correction for multiple comparisons. (* p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001).