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. 2019 Jan 18;10(6):647–659. doi: 10.18632/oncotarget.26567

Figure 1. Increased sensitivity of SETD2 deficient ccRCC-derived cells to PI3Kβ-specific inhibitors.

Figure 1

(A) Bar graph showing relative cell viability as a percentage of CTL (DMSO-treated) of SETD2 proficient (+/+) 786-0 and SETD2 deficient (KO) 786-0 and (–/–) A498 cells in response to treatment with small-molecule inhibitors. *P < 0.05; **P < 0.005; ***P < 0.001; ****P < 0.0001; ns, no statistical significance. Standard deviations were calculated and represented for all conditions. (B) Dose-response curves showing sensitivity to AZD8186, BYL719, Idelalisib, and BKM120 at different concentrations. IC50 was calculated for each treated cell line with a non-linear fit of transformed values using GraphPad software. (C) Western blot analysis of indicated proteins showing variations in phosphorylation levels in response to chemical inhibition. Whole-cell protein lysates from cells treated with 1 μM inhibitor for 24 hours were resolved by SDS-PAGE. Actin is a loading control.