Extended Data Fig. 7: ENO2-derived PEP increases β-catenin acetylation and transcriptional activity in CRC cells.
a, b, LC-MS/MS analysis was conducted to determine the concentrations of intracellular PEP in (a) antiangiogenic drug-sensitive and -resistant HCT116 cells, and (b) CRC cells treated without or with PEP (n = 3). Bev, bevacizumab. Rego, regorafenib. (a, b, n = 3 biologically independent experiments). c, The expression of Ac-K49-β-catenin in CRC cells treated with a gradient concentration of PEP was determined by Western blotting. Representative of n = 3 independent replicates. d, TOP/FOP Flash reporter assay was performed to assess the effect of PEP on β-catenin transcriptional activity in HCT116 cells. n = 3 biologically independent experiments. e–g, Western blotting was performed to evaluate the effect of PEP on (e) β-catenin phosphorylation and (f, g) the expression of β-catenin target genes (c-Myc and Cyclin D1) in CRC cells. Representative of n = 3 independent replicates. Data are presented as the mean ± s.e.m. P values were determined by one-way ANOVA with Tukey’s multiple comparison test (a, b and d).
