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. 2008 Jun 4;28(23):5870–5878. doi: 10.1523/JNEUROSCI.5385-07.2008

Figure 2.

Figure 2.

Expression of activated STAT3 inhibits proliferation PTEN-deficient glioblastoma cells. A, Schematic of activated STAT3 (S3C) or a DNA-binding mutant version of S3C (mS3C). B, Left, Lysates of U87 glioblastoma cells infected with a control retrovirus containing an IRES-GFP cassette or retroviruses that also encode FLAG-tagged S3C or mS3C were immunoblotted with STAT3 and FLAG antibodies and antibodies to STAT1 or Akt as loading controls. Right, Cell population growth curves of U87 glioblastoma cells. S3C-expressing U87 cells proliferated significantly more slowly than mS3C-expressing U87 cells or those infected with control virus (n = 3; ANOVA, *p < 0.05). C, BrdU labeling of U87 glioblastoma stable cells measured as a percentage of the total number of cells. Incorporation of BrdU was significantly reduced in U87-S3C cells compared with both vector and mS3C (n = 4; ANOVA, *p < 0.05). D, Cell population growth curves of PTEN-deficient U87 cells or isogenic PTEN-expressing U87 cells infected with the S3C or control retrovirus. Expression of S3C significantly reduced the proliferation of U87 but not of isogenic PTEN-expressing U87 glioblastoma cells (representative experiment of 3 independent experiments performed in triplicate; ANOVA, *p < 0.001, **p < 0.0001).