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. 2014 Jul 1;35(9):2142–2153. doi: 10.1093/carcin/bgu143

Fig. 3.

Fig. 3.

Intratumoral heterogeneity in PTEN-deficient mouse prostate cancer. (A) Expression of AR, phosphorylated (p-AKT, p-S6, p-ERK1/2, p-STAT3-(pY705) and p-STAT3-(pY727)) and total protein (AKT, S6, ERK1/2 and STAT3) in pooled prostate tumor lysates (three mice per group) collected from castration-naive wild-type and PTEN-deficient mice at indicated ages. Original blots are included in Supplementary Figure 8, available at Carcinogenesis Online. (B) Densitometric analysis of (A). (C) Representative images showing the histological and IHC staining patterns of key downstream pathways molecules in advanced castration-naive mouse prostate cancer at 72 weeks of age. Inserts correspond to boxed region, scale bars represent 100 μm. (D) Expression of phosphorylated (p-AKT, p-S6, p-ERK1/2, p-STAT3-(pY705) and p-STAT3-(pY727)) and total protein (AKT, S6, ERK1/2 and STAT3) in individual 20-week-old mice with castration-naive and CRPC. glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as a loading control. Original blots are included in Supplementary Figure 9, available at Carcinogenesis Online. (E) Densitometric analysis of (D, *P ≤ 0.05 versus castration-naive cancer). (F) Representative H&E staining and IHC expression analysis of AR, p-AKT, p-S6, p-ERK1/2, p-STAT3-(pY705) and p-STAT3-(pY727) in prostate tumors from (D), scale bars represent 250 μm. Protein levels were normalized to GAPDH or total protein for all densitometric analyses.