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. 2022 Oct 21;9(34):2202528. doi: 10.1002/advs.202202528

Figure 2.

Figure 2

NU2058 disturbs the nuclear translocation of β‐catenin. A) The total β‐catenin level was detected in NU2058‐treated (0, 10, and 20 µm, 72 h) CRC cells. B) Subcellular fractionation and Western blotting were used to assess the expression of β‐catenin in the nucleus and cytoplasm of CRC cells exposed to the indicated concentrations of NU2058. C) Immunofluorescent staining showing the subcellular localization of β‐catenin in CRC cells treated with NU2058 (0 and 20 µm, 72 h). D) qRT–PCR was used to detect the mRNA levels of cyclin D1 and c‐Myc in NU2058‐treated CRC cells. E) Design of the mutated cyclin D1 and c‐Myc promoters. Dual luciferase reporter assay was performed to detect the effect of NU2058 on the activity of the cyclin D1 or c‐Myc promoter in CRC cells. F) Western blotting showing that cyclin D1 and c‐Myc expression was inhibited by NU2058 (0, 10, and 20 µm) in DLD1 and HCT15 cells. G) Western blotting analysis of cyclin D1 and c‐Myc expression in NU2058‐treated tumor xenografts. H) WST‐1 assay illustrating that forced expression of β‐catenin in RKO cells increased their sensitivity to NU2058 (0, 10, and 20 µm, 72 h). I) Detection of the expression of β‐catenin in the nucleus and cytoplasm of β‐catenin‐overexpressing RKO cells. J) WST‐1 assay illustrating that knocked down of β‐catenin in DLD1 and HCT15 cells abolished their sensitivity to NU2058 (72 h). Bars, SD; *p < 0.05; **p < 0.01; ***p < 0.001.