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. 2016 Jun 17;7(33):53047–53063. doi: 10.18632/oncotarget.10132

Figure 2. Modulation of multipotency, differentiation and survival markers in PDGFRα-depleted GBM CSC vs control cells.

Figure 2

A. Western blot analysis reveals that depletion of PDGFRα in p-CSC2 induces the downmodulation of Stat3 Y705 phosphorylation in both proliferating cell clones, instead their levels raised up in differentiation conditions. The hypo-Rb1 levels result overexpressed in clone 3 in all conditions. Instead the clone 1, shows an increase of hypo-Rb1 at 2 and 4 day of differentiation with respect to pLKO.1 cells. In parallel, Bcl-2 and Bcl-xL proteins and Erk1/2 pathway were upregulated in both cell clones in comparison with pLKO.1 cells in differentiaton conditions. T638/641 phosphorylated-PKCα/βII isoforms expression levels are slightly induced in proliferating PDGFRα-depleted cell clones, but negatively modulated in differentiated ones than pLKO.1 cells. B. The downmodulation of multipotent protein markers (Nestin, Sox2, Bmi1), except for Oct4, is accompanied with early induction of the neuronal marker MAP2a/b in proliferating PDGFRα-depleted cell clones vs pLKO.1. Similar results were observed during cell differentiation, except for MAP2a/b that increases in pLKO.1 with respect to PDGFRα-depleted cells.