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Dual inhibition of oxidative phosphorylation and glycolysis exerts a synergistic antitumor effect on colorectal and gastric cancer by creating energy depletion and preventing metabolic switch

Fig 2

Effect of OXPHOS and glycolytic inhibition on tumor growth in HCT116 and MKN45 xenografts.

(A) HCT116 cells (5×106) were subcutaneously injected into the back of athymic nude. mice. After the size of the subcutaneous tumor reached 100 mm3, NCI-006 (40 mg/[kg•dose] body weight, red arrowheads) was administered intravenously thrice a week, and IACS-010759 (20 mg/[kg•dose] body weight, green arrowheads) was administered orally every day for a week. Data are displayed as means ± standard error of the mean (SEM) (n = 12 for each group; *p < 0.05, **p < 0.01, two-way ANOVA Tukey test). (B) MKN45 xenograft mice were generated as described in (A). NCI-006 (40. mg/[kg•dose] body weight, red arrowheads) was administered intravenously twice a week, whereas IACS-010759 (20 mg/[kg•dose] body weight, green arrowheads) was administered orally five times a week for two weeks. Data are displayed as means ± SEM (n = 6 for each group; *p < 0.05, **p < 0.01, two-way ANOVA Tukey test). (C) The body weight change of the mice in the experiment (A). (D) The body weight change of the mice in the experiment (B). Abbreviation: IACS, IACS-010759.

Fig 2

doi: https://doi.org/10.1371/journal.pone.0309700.g002