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Fig. 1 | Breast Cancer Research

Fig. 1

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

Fig. 1

Early TNBC cell lines exhibit different basal glycolytic activities. A, B Growth of HCC1143, HCC38 and HCC1937 TNBC cell lines after treatment with increasing concentrations of epirubicin (A) or paclitaxel (B) for 72 h. C Calculated IC50 values and 95% confidence intervals for epirubicin and paclitaxel in TNBC cell lines. D–E Growth of HCC1143, HCC38 and HCC1937 TNBC cell lines after treatment with IC50 of epirubicin (D) or paclitaxel (E) for 24 h and then for 48 h upon drug withdrawal (washout). F Extracellular acidification rates (ECAR) in HCC1143, HCC38 and HCC1937 cells upon sequential treatment with 10 mM glucose, 1 µM oligomycin and 50 mM 2-deoxyglucose (2-DG). G–H Glucose-dependent (G) and maximal ECAR (H) in HCC1143, HCC38 and HCC1937 cells. I–J Glucose consumption (I) and lactate secretion (J) in HCC1143, HCC38 and HCC1937 TNBC cell lines. K Representative immunoblotting for HK2, GAPDH and LDHA in HCC1143, HCC38 and HCC1937 cells. L Quantification of LDHA protein levels in HCC1143, HCC38 and HCC1937 cells. Data are plotted as the means ± SEM from n = 3–6 cultures, performed each time with ≥ 3 technical replicates (A, B, D–J and L). Significance was determined by one-way ANOVA with Tukey’s multiple comparison test (G–J and L). *p < 0.05; ***p < 0.001; ns, not significant

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