Fig. 6 Zic5 regulates glucose metabolism in a β-catenin/Tcf7l2–dependent manner in HCT116 colon cancer cells. Zic5 regulates glucose metabolism in a β-catenin/Tcf7l2–dependent.

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Fig. 5 Correlation of RNA expression and protein abundance.

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Fig. 6 Zic5 regulates glucose metabolism in a β-catenin/Tcf7l2–dependent manner in HCT116 colon cancer cells. Zic5 regulates glucose metabolism in a β-catenin/Tcf7l2–dependent manner in HCT116 colon cancer cells. (A) Zic5 KO cells (C18) were infected with three independent shRNAs against Zic2. Western blot showed the knockdown efficiency of Zic2 knockdown after puromycin selection. HCT116 parental cells were included as positive control. (B) RNA-seq tracks showed the GLUT1/SLC2A1 gene expression decrease with Zic2 knockdown. (C) Western blot showing the cleaved PARP levels of Zic2 knockdown in Zic5 KO cells cultured in the DMEM medium with high (H, 25 mM) or low glucose (L, 0.5 mM). (D) Glucose uptake in Zic5 KO cells with shCtrl of shZic2 is measured by 2-NBDG uptake. The fluorescence intensity is quantified by the plate reader (n = 8). ***P < 0.001. (E) Venn diagram analysis identifies 58 common genes by Zic2 knockdown and Zic5 KO. The P value was determined with the hypergeometric test. (F) Zic5 acts as a transcriptional repressor in regulating SLC2A1/GLUT1 gene expression. Loss of Zic5 derepresses GLUT1 gene expression and further increases the protein level of GLUT1. Glucose uptake is increased and thus leads to the more glycolytic features of the cells. This may link to the tumor progression in the tumor microenvironment. Zibo Zhao et al. Sci Adv 2019;5:eaax0698 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).