Research Paper Volume 2, Issue 11 pp 823—842

A STAT3-mediated metabolic switch is involved in tumour transformation and STAT3 addiction

class="figure-viewer-img"

Figure 1. Phenotype of the Stat3C/C MEFs. Primary MEFs were derived from Stat3C/C or Stat3WT/WT embryos and experiments performed on at least three independent samples per genotype. (A) Constitutive nuclear localization of STAT3C. Cells of the indicated genotypes were treated or not with IL-6 and stained for total or tyrosine-phosphorylated STAT3. Nuclei are stained in blue with Hoechst. (B) Increased growth rates. 1.5*105 cells were plated and counted at the indicated times. Data are mean cell numbers ± s.e.m.. (C) Apoptosis protection. Cells were treated with H2O2 for 16 hours, photographed in phase contrast and stained with Annexin V. Numbers represent the percentage ± s.e.m. of Annexin V positive cells. (D) Delayed senescence. Phase contrast: note different viability at 0 and 3 weeks post-confluence. X-Gal: β-galactosidase activity assessed at 3 and 6 weeks post-confluence. Stat3WT/WT cells were all dead at 6 weeks. (E) Decreased ROS production. Cells were regularly passaged and intra-cellular ROS production measured at passage (P) 1, 3 or 4.