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. Author manuscript; available in PMC: 2016 Jan 29.
Published in final edited form as: Cell. 2015 Jan 15;160(3):393–406. doi: 10.1016/j.cell.2014.12.018

Figure 3. CKB modulates colorectal cancer cell survival during acute intrahepatic hypoxia through modulation of the phosphocreatine/ATP shuttle.

Figure 3

A, Relative intracellular phosphocreatine levels in SW480 cells over-expressing CKB or depleted for CKB (n=5). B, Relative intracellular ATP levels in LvM3b cells depleted for CKB, with and without exogenous 10um phosphocreatine supplementation (n=5). C, In vivo caspase activity of control and CKB knockdown SW480 cells experiencing hypoxia within the livers of mice (n=3). D, Survival of colorectal cancer cells in hypoxia in vitro with and without CKB knockdown, and 10um phosphocreatine supplementation (n=3). E, Liver metastasis by CKB depleted LvM3b cells pre-incubated overnight with 10um phosphocreatine. 5 × 105 cells were then inoculated into the liver of mice through intrasplenic injection. F, Liver metastasis in mice injected with 5 × 105 LvM3b cells with and without pre-treatment with 10mM cyclocreatine for 48hrs. Error bars, s.e.m; all p values are based on one-sided Student’s t-tests, or where appropriate, Mann-Whitney test for non-Gaussian distribution. *p<0.05; **p<0.01; ***p<0.001. See also Figure S3.