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Fig.  2 | Breast Cancer Research

Fig.  2

From: Metabolic adaptation towards glycolysis supports resistance to neoadjuvant chemotherapy in early triple negative breast cancers

Fig.  2

Paclitaxel and epirubicin induce opposite effects on glycolytic activity in TNBC cells. A, B Glucose consumption (A) and lactate secretion (B) in HCC1143 cells upon treatment with 9 nM paclitaxel or 600 nM epirubicin for 72 h. C, D ECAR profile upon sequential treatment with 10 mM glucose, 1 µM oligomycin and 50 mM 2-DG (C) and glucose-dependent ECAR (D) in HCC1143 cells treated with 9 nM paclitaxel or 600 nM epirubicin for 24 h. E, F Glucose consumption (E) and lactate secretion (F) in HCC38 cells upon treatment with 4 nM paclitaxel or 25 nM epirubicin for 72 h. G, H ECAR profile upon sequential treatment with 10 mM glucose, 1 µM oligomycin and 50 mM 2-DG (G) and glucose-dependent ECAR (H) in HCC38 cells treated with 4 nM paclitaxel or 25 nM epirubicin for 24 h. I, J Representative immunoblotting (I) and quantification (J) for HK2, GAPDH and LDHA in HCC1143 and HCC38 cells upon treatment with 9 or 4 nM paclitaxel, respectively, and 600 or 25 nM epirubicin, respectively for 72 h. Data are plotted as the means ± SEM from n = 2–6 cultures, performed each time with ≥ 3 technical replicates (A–H, and J). Significance was determined by one-way ANOVA (A, B, D–F, and H) or two-way ANOVA (J) with Tukey’s multiple comparison test. *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant

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