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. 2017 Dec 11;32(6):840–855.e8. doi: 10.1016/j.ccell.2017.11.005

Figure 1.

Figure 1

Increased Expression of STK26 Correlates with Tumorigenicity and Prognosis in GBM

(A) Heatmaps showing the top and bottom 50 most differentially expressed genes or kinase-encoding genes in PN and MES GSCs, neural progenitors, and normal astrocytes (GEO: GSE67089).

(B) Immunoblot (IB) for MST4 and β-actin in indicated GSCs.

(C) H&E (upper) and bioluminescent (BLI, lower) images of indicated GSC brain tumor xenografts. Colors in the BLI images indicated the strength/intensity of BLI signals: red, strong; cyan, intermediate; and blue, weak. Length of time between transplantation and tissue collection is shown below. Red triangle at the bottom indicates the increasing tumor growth ability of GSCs. Scale bars, 1.0  mm.

(D) Comparison of STK26 expression levels between GBM, low-grade glioma (LGG) and normal brain tissues.

(E) Comparison of STK26 expression levels between GBM MES, PN, or CL subtypes.

(F and G) Kaplan-Meier survival analyses for STK26 expression (F) and STK26 expression and IDH1 status (G).

Data in (B) and (C) are representative of two independent experiments with similar results. Box plots in (D) and (E) indicate the median and upper and lower quartiles, with whiskers extending to the minimum and maximum range. Data in (D) to (G) were generated by analysis of a TCGA RNA-sequencing dataset (Tables S2–S4). ∗∗∗p < 0.0001. See also Figure S1 and Tables S1–S6.