Fig. 1
From: STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway
Loss of STAT3 accelerates metastatic progression and exhibits decreased LKB1/AMPK signaling. A High occurrence of PTEN and STAT3 deletions in plasma samples of PCa patients with aggressive PCa (n = 95). B Kaplan–Meier cumulative survival analysis revealed a significant (p = 0.0026; log-rank test) increase in lifespan of Ptenpc−/−Stat3C/+ compared to Ptenpc−/−Stat3pc−/− mice; WT and Ptenpc−/− mice served as controls (n = 68). C Prostate weights of 19-week-old WT, Ptenpc−/−, Ptenpc−/−Stat3pc−/− and Ptenpc−/−Stat3C/+ mice (n = 99). Mean values are shown; Data were analyzed by one-way analysis of variance with Tukey’s multiple comparison test; error bars: s.d. D IHC of muscle and mesentery, 52 weeks of age WT, Ptenpc−/−, Ptenpc−/−Stat3C/+ and Ptenpc−/−Stat3pc−/− mice. MET- metastasis, Scale bars, 100 μm; insets: × 600 magnification. Percentage of mice with distant PCa metastases (n = 76). E Haematoxilin/eosin (H&E) stains show only high-grade PIN in Ptenpc−/−Stat3C/+ mice compared with Ptenpc−/− and Ptenpc−/−Stat3pc−/− mice. Scale bars, 100 μm. IHC analysis of Stat3, Lkb1 and p-Ampk in prostates from 19-week-old WT, Ptenpc−/−, Ptenpc−/− Stat3pc−/− and Ptenpc−/−Stat3C/+ mice. Scale bars, 100 μm. Bar graphs indicate percentage of cells positive for Stat3, Lkb1 and p-Ampk in prostates of 19-week-old WT, Ptenpc−/−, Ptenpc−/−Stat3pc−/− and Ptenpc−/−Stat3.C/+. Protein levels quantification was done with HistoQuest software (n ≥ 3)