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Fig. 5 | Journal for ImmunoTherapy of Cancer

Fig. 5

From: Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFNγ receptor signaling

Fig. 5

IFNy 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 < 0.001

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