Cancer cells are capable of sustaining proliferative signalling and resisting cell death. To be able to maintain enhanced proliferation, cancer cells have higher energy demands, which are in part satisfied with increased rates of glucose transport across the cell membrane. GLUT1 is a glucose transporter whose expression levels are elevated in various types of cancer cells. As a consequence, GLUT1 is perceived as a potential target in targeted cancer therapy. Several articles report that cancer treatment with already established chemotherapeutic agents has a synergistic effect in combination with GLUT1 inhibition. The aim of our work was to investigate whether GLUT1 affected the viability of 4T1 cancer cells in the presence of staurosporine and doxorubicin. We used 4T1 cells with a knocked out gene that encodes for GLUT1 to mimick complete inhibition of the transporter. Differences in genotype and phenotype of control and knockout cells was confirmed with qPCR and western blot. The viability of cells was assessed with bioluminescence and MTT assays. We confirmed that even in the absence of chemotherapeutic agents Slc2a1 knockout results in a significant decrease in proliferation of 4T1 cells. However, the absence of GLUT1 does not display synergistic effects with staurosporine and doxorubicin. Staurosporine equally affected control and knockout cells, whereas doxorubicin had a smaller effect on knockout cells even though their proliferation rates were still lower than those of the control cells.
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