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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Cell Metab. 2015 Jul 16;22(3):508–515. doi: 10.1016/j.cmet.2015.06.009

Figure 4. Inherent vulnerability, or the loss of cell viability, characteristic of cells with ATP5B knockdown, 2-HG accumulation, or IDH mutations.

Figure 4

(A) U87/IDH1(R132H) cells have increased vulnerability to glucose starvation (***P < 0.001).

(B-D) Octyl α-KG or octyl 2-HG treated U87 cells exhibit decreased viability upon glucose starvation (****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05).

(E) ATP5B knockdown inhibits U87 cell growth (***P = 0.0004).

(A-E) Cells were cultured in galactose medium.

(F) HCT 116 IDH1(R132H/+) cells exhibit increased vulnerability to glucose-free medium supplemented with (R)-3-hydroxybutyrate (***P < 0.001).

(G-I) U87 cells with ATP5B knockdown or octyl esters of α-KG or 2-HG treatment and HCT 116 IDH1(R132H/+) cells exhibit decreased mTOR Complex 1 activity in glucose-free, galactose-containing medium. All lanes in (I) are on the same blot; space indicates position of unnecessary lanes that were digitally removed. Octanol has no effect on mTOR activity.

(A-F) By unpaired t-test, two-tailed, two-sample unequal variance. Mean ± s.d. is plotted. (A-I) Results were replicated in at least two independent experiments.