Fig. 8
From: p66ShcA functions as a contextual promoter of breast cancer metastasis
Non-mitochondrial p66ShcA pools activate the AKT/mTOR pathway in breast tumors. a Whole-cell lysates were generated from the indicated cell lines grown under the following conditions: 10% FBS versus 0% FBS for 16 h; 1 mM phenformin for 2 h; 20 μM sodium arsenate for 4 h; suspension cultures on ultra-low attachment plates for 16 h. Immunoblot analysis was performed using the indicated antibodies. b Percentage of p37/46-4EBP1 and pS240/244-rS6 positive pixels in primary breast tumors (n = 8 tumors/genotype) and in individual lung-metastatic lesions derived from 4T1-537 p66-CR (VC), p66-CR (WT), and p66-CR (S36A) breast cancer cells. For the lung metastases: p66-CR (VC), n = 235 lesions (p4EBP) and n = 306 lesions (p-rS6); p66-CR (WT), n = 202 lesions (p4EBP) and n = 315 lesions (p-rS6); p66-CR (S36A), n = 237 lesions (p4EBP) and n = 305 lesions (p-rS6). Statistical analysis was performed using a one-way ANOVA with a Tukey’s multiple comparisons test (**P < 0.01; ***P < 0.001; ****P < 0.0001). c Representative IHC images for the data shown in panel b are shown