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Fig. 3 | Radiation Oncology

Fig. 3

From: Role of SGK1 for fatty acid uptake, cell survival and radioresistance of NCI-H460 lung cancer cells exposed to acute or chronic cycling severe hypoxia

Fig. 3

SGK1 inhibition abrogates the rescue effect of oleic acid. Oxic and anoxia-tolerant NCI-H460 cells were treated with the SGK1 inhibitor GSK650394 (40 μM) under serum-deprived conditions with or without supplementation of oleic acid (5 mM) for 24 h under normoxic (20 % O2) or severely hypoxic conditions (0.2 % O2). a Representative light microscopic pictures of oxic and anoxia-tolerant NCI-H460 cells 72 h after the indicated treatment under normoxic or severely hypoxic conditions. Scale bar = 10 μM. b Number of viable cells determined by crystal violet assay 72 h after the indicated treatments in normoxia (upper panel) or severe hypoxia (lower panel). c, d Cell death was quantified 72 h after treatment by flow cytometry as described in Fig. 2. The increase in cell death levels by a particular treatment was visualized in a heat map representing fold changes in normoxia (c, lower panel) and severe hypoxia (d, lower panel). SGK1 inhibition by GSK650394 decreased cell viability and increased the amount of dead cells in both cell lines under normoxic (b upper panel, c) and severely hypoxic conditions (b lower panel, d). Cell death induction was more prominent in anoxia-tolerant NCI-H460 cells (c lower panel, d lower panel). SGK1 inhibition abrogates the rescue effect of supplementation with oleic acid (50 μM) on serum deprivation induced cell death under severely hypoxic conditions (b-d). Mean values ± SD are shown, n = 3. (* p ≤ 0.05, *** p ≤ 0.001; two-way ANOVA with Bonferroni post-test)

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