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. Author manuscript; available in PMC: 2020 Feb 8.
Published in final edited form as: Clin Cancer Res. 2017 Nov 27;24(5):1216–1226. doi: 10.1158/1078-0432.CCR-17-0824

Figure 4. Recombinant t-Darpp confers an IGF-1R-dependent increase in glycolysis.

Figure 4.

(A) Seahorse analysis of ECAR at baseline in 1mM glutamine, 1mM pyruvate without glucose and following injection of 16mM glucose (Medium) or glucose supplemented with 500nM recombinant t-Darpp (t-Darpp). (B) SK-BR-3 cells were pre-treated in media minus or plus 5µM NVP-AEW for one hour. ECAR was analyzed at baseline in 1mM glutamine, 1mM pyruvate and 16mM glucose and following injection of medium supplemented with 500nM recombinant t-Darpp, the data is presented as net change in ECAR following injection. (C) Western blot analysis of IGF-1R and Akt phosphorylation following treatment with recombinant t-Darpp protein (left) and the effect of IGF-1R inhibition with NVP-AEW prior to treatment with recombinant t-Darpp (right) Numbers indicate fold change compared to untreated samples after normalization to total protein (D) Western analysis comparing Akt phosphorylation following treatment with recombinant t-Darpp (400nM), an inhibitory IGF-1R monoclonal antibody (Ab) or both. (E) Percent change in ECAR following treatment with 500nM recombinant t-Darpp of a panel of breast cancer cell lines (SK-BR-3, BT474, T47D, MCF7, HCC1937 and MDA-MB-231). Shown is the mean change in ECAR normalized to untreated controls (n=3–6). *p<0.05, **p<0.01 ***p<0.001 ****p<0.0001