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. Author manuscript; available in PMC: 2017 Mar 28.
Published in final edited form as: Cell Rep. 2017 Feb 28;18(9):2243–2255. doi: 10.1016/j.celrep.2017.02.013

Figure 3. Dormant cancer cells lacking oncogenic KRAS exhibit a compensatory increase in IGF-1R/AKT signaling.

Figure 3

A. Heat map of genes that cluster with IGF1 signaling and that exhibit a deregulated expression in residual cancer cells following compared to pancreatic bulk tumors. B. Immunohistochemical staining of the activated IGF1 receptor (pIGF-1R) as well as pAKT in oncogenic KRAS-expressing bulk tumor cells and in residual cancer cells two weeks after the ablation of the oncogene; bar represents 50 μm. C. Immunoblot analysis comparing the expression and activation of IGF-1R and AKT as well as levels of downstream regulators of cell survival and cell death between bulk tumors and residual cancer tissues; cCASP3, cleaved Caspase 3. Bar graphs show Image-J quantification of selected protein bands. All data are represented as mean ± SEM; * represents P<0.05.