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Correction to: Cellular Oncology
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Fig. 4 Wild-type IDH2 elevates glucose uptake and GLUT1 expression via NF-κB signaling in CRC cells. a IDH2 overexpression enhances glucose uptake. 2-NBDG in CRC cells was determined with a fluorescent microscope and a microplate reader (Ex/Em 476/550 nm). Data from at least 3 replicates, and p values were determined by unpaired t-test. (* p < 0.05). b IDH2 increases the expression of GLUT1 on the cell surface. Representative pictures of GLUT1 expression detected by confocal microscope after immunostaining. c IDH2 overexpression upregulates GLUT1 expression but not GLUT4. The phosphorylation of NF-κB p65 and IκBa, and the degradation of IκBa were determined by Western blotting. Representative figures are shown. Data are representative of at least three independent experiments. d IDH2 knockdown cells SW480 or HCT116 were treated with Octyl-2 KG (0.5 mM) for 16 h. Western blotting determined the expression of GLUT1, GLUT4, and NF-kB signaling molecules. Representative figures are shown. Data are representative of at least three independent experiments
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He, X., Wu, N., Li, R. et al. Correction to: IDH2, a novel target of OGT, facilitates glucose uptake and cellular bioenergy production via NF-κB signaling to promote colorectal cancer progression. Cell Oncol. 46, 165–166 (2023). https://doi.org/10.1007/s13402-022-00764-8
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DOI: https://doi.org/10.1007/s13402-022-00764-8