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. 2015 Apr 14;6(13):10728–10745. doi: 10.18632/oncotarget.3828

Figure 3. Chemotherapy increases glycolytic function of hTERT-BJ1 fibroblasts and transforms them into less metabolically efficient cells.

Figure 3

A. hTERT-BJ1 fibroblasts were treated for 72 h with carboplatin, B. azathioprine, doxorubicin, mitoxantrone, taxol and C. cisplatin before the extracellular efflux assay was performed. All drugs increased the ECAR of hTERT-BJ1 cells throughout the experiment compared to vehicle treatments. Mean ± SEM. D. Glycolysis, glycolytic capacity and glycolytic reserve measurements of chemotherapy-treated hTERT-BJ1 fibroblasts relative to vehicle-treated cells. All drugs significantly increased glycolytic capacity, and most of them also augmented the glycolytic reserve of hTERT-BJ1 fibroblasts (except cisplatin). Likewise, basal glycolytic rate was enhanced in carboplatin, doxorubicin, mitoxantrone and taxol treatments. Mean ± SEM. E. hTERT-BJ1 fibroblasts were treated for 72 h with carboplatin, F. azathioprine, doxorubicin, mitoxantrone, taxol and G. cisplatin before the extracellular efflux assay in the presence of glucose was performed, and the OCR versus ECAR graph was represented. All drugs induced a shift towards a less metabolically active phenotype in hTERT-BJ1 cells. Mean ± SEM.