Fig. 5From: Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFNγ receptor signalingIFNy responsiveness of metabolically stressed tumor cells can be restored by PI3K inhibition. Tumor cells were cultured under normal, GD, OD, or OGD conditions together with IFNy for 24 h. a and c Western-blots of TC1 (a) and B16F10 (c) tumor cells. Representative data out of three experiments is shown. b and d Quantification of western-blot results of phospho-AKT expression in TC1 (b) and B16F10 (d) tumor cells. e and g TC1 (e) and B16F10 (g) tumor cells were cultured under normal or OGD conditions with or without LY294002 for 24 h. Representative western-blot results out of three experiments is shown. f and h Quantification of western-blot results of phospho-AKT expression in TC1 (f) and B16F10 (h) tumor cells. i and k Western-blots of TC1 (i) and B16F10 (k). Phospho-STAT1 and IRF-1 expression levels are shown. j, l, m and n Quantified data of (i and k). Data was quantified by calculating signal ratio between protein of interest and beta-actin. Unpaired t test was used to calculate significance; n.s., not significant *, p < 0.05, **, p < 0.01, ***, p < 0.001Back to article page