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. 2015 Jan 31;6(9):7293–7304. doi: 10.18632/oncotarget.3421

Figure 1. Plexin-B2 is upregulated in glioma.

Figure 1

A) Relative Plexin-B gene expressions in glioma vs. normal brain from microarray data of four patient studies (B, Bredel et al. (n=49); S, Sun et al. (n=49); T, TCGA (n=424); R, Rembrandt (n=454)). Whiskers show top and bottom quartiles. PLXNB2 was upregulated in all four glioma studies. B) Relative PLXNB2 expression in four molecular subtypes of glioblastoma (TCGA dataset; proneural, n=113; neural, n=70; classical, n=112; mesenchymal, n=128). C) Abundance of Plexin-B and Sema4 mRNA in TCGA glioblastoma samples (n=169), shown as RSEM counts (upper quartile boundary normalized to 1000). PLXNB2 exhibited the highest mean abundance level overall, and SEMA4B, 4C and 4D exhibited higher levels than other Sema4s. D) PLXNB2 mean expression is significantly increased in all WHO glioma types (NCI/Rembrandt patient cohort; n=454; probeset 208890_s_at) and highest in glioblastoma (p<0.001). E) Western blot of nine surgical samples from glioma patients reveals robust Plexin-B2 protein expression (170 kDa band is the processed, mature form of Plexin-B2). Normal human cortex served as control. Plexin-B1 and -B3 protein are variably expressed among glioma samples.