Figure 6.

Genetically targeting β8 integrin in low-passage GBM cells leads to defective tumor initiation in vivo. (a) Immunoblot analysis showing absence of β8 integrin protein expression in β8^KO cells generated via Crispr-Cas9 gene editing strategies. (b, c) FACS plot from β8^WT (b) and β8^KO (c) GBM cells, revealing loss of β8 integrin protein expression on the GBM cell surface. (d, e) Images of H&E-stained tumor sections from mice injected with β8^WT GBM cells, revealing larger and more invasive tumors derived from β8^WT cells. (f, g) Immunofluorescence analysis of xenograft tumors derived from β8^WT GBM cells. The anti-vimentin antibody (green) is specific for human cells and anti-nestin (red) labels neural stem cells. (h, i) Brain sections from mice injected with β8^KO GBM cells were stained with H&E, revealing small and minimally invasive tumors. (j, k) Immunofluorescence analysis with anti-vimentin and anti-nestin antibodies of mouse brains injected with β8^KO GBM cells. Note that there are fewer human cells in β8^KO-derived tumors as revealed by anti-vimentin immunofluorescence staining. All scale bars are 10 μm.