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. Author manuscript; available in PMC: 2012 Jun 1.
Published in final edited form as: Nature. 2011 Dec 1;480(7375):118–122. doi: 10.1038/nature10598

Figure 4. The PKM2–β-catenin interaction is required for tumor development.

Figure 4

a, b, U87, U87/EGFRvIII cells with or without depleted β-catenin and reconstituted expression of rβ-catenin (a), or U87/EGFRvIII cells with or without depleted PKM2 and reconstitution of the expression of rPKM2 (b), were plated and counted 7 days after seeding. Data represent the means ± SD of three independent experiments.

c, U87 (bottom left panel), U87/EGFRvIII cells with or without depleted β-catenin and reconstituted expression of rβ-catenin (top panel), or U87/EGFRvIII cells with or without depleted PKM2 and reconstituted expression of rPKM2 (bottom right panel) were intracranially injected into athymic nude mice. After two weeks, tumor growth was examined. H&E-stained coronal brain sections show representative tumor xenografts.

d, IHC staining with the indicated antibodies was performed on 55 GBM specimens. Representative photos of four tumors are shown.

e, f, The survival time for 84 patients with low (0-5 staining scores, blue curve) versus high (6-8 staining scores, red curve) β-catenin Y333 phosphorylation (e; low, 28 patients; high, 56 patients) and nuclear PKM2 expression (f; low, 28 patients; high, 56 patients) were compared (bottom panel). The table (top panel) shows the multivariate analysis after adjustment for patient age, indicating the significance level of the association of Y133-phosphorylated β-catenin expression (e) or nuclear PKM2 expression (f) with patient survival. Empty circles represent the deceased patients, and filled circles represent the censored (alive at last clinical follow-up) patients.