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. 2021 Mar 25;13(7):1518. doi: 10.3390/cancers13071518

Figure 1.

Figure 1

Confirmation of lactate calcium salt (CaLac) influx into colorectal cancer (CRC) cells under hypoxia. (A) Schematic illustration of the direct effects of CaLac on anaerobic glycolysis under hypoxia. A large amount of glucose is influx into hypoxic cancer cells and converted to pyruvate via hexokinase [16]. The pyruvate is converted to lactate through lactate dehydrogenase A (LDHA) and outfluxed from the cancer cell. However, activation of LDHB by CaLac reduces the action of LDHA (Figure S2) and leads to an increase in pyruvate from CaLac. (B) Immunofluorescence calcium imaging following 2.5 mM CaLac treatment in HCT116 cells. Scale bars, 200 μm (C) Quantitative intracellular calcium levels following 2.5 mM CaLac treatment in CRC cells; 2 × 106 cells were analyzed respectively. (D) Intracellular lactate levels following 2.5 mM CaLac treatment in CRC cells. 2 × 106 cells were analyzed respectively. ** p < 0.001 vs. Untreated. Results are represented as mean ± standard deviation.