Wei L, Li P, Luo Y, et al. Onco Targets Ther. 2020;13:10025—10037.
The authors have advised Figure 4 on page 10033 is incorrect due to errors at the time of figure assembly. Part A, second panel, the label “DVL2, p-DVL2” should read “p-DVL2, DVL2”, and the last panel in part E is missing a label. The correct Figure 4 is shown below.
Figure 4.
PWP1 activates the Wnt signaling pathway by interaction with DVL2. After transfection of PWP1 into SK-MES-1 cell line, wb showed that the phosphorylation of DVL2 and Active β-catenin were upregulated, and the expression levels of target genes of Wnt pathway, C-myc, Cyclin D1 and MMP7 were upregulated (A). After knocking down of PWP1 into H1299 cell line, wb showed that the phosphorylation of DVL2 and Active β-catenin were downregulated, and the expression levels of target genes of Wnt pathway, C-myc, Cyclin D1 and MMP7 were downregulated (B). GAPDH serves as a loading control. The grey value was measured using Image software. Luciferase gene-reporter assays showed that PWP1 could activate the Wnt pathway, after knocking down PWP1, the Wnt pathway would be inhibited (C). Columns: mean numbers, Bar: SD. (*P<0.05). PWP1 and DVL2 co-localized in the cytoplasm (D, magnification 600×). Co-ip testing confirmed the interaction between PWP1 and DVL2 (E). Transfection of PWP1 and knocking down DVL2 would offset the effects of PWP1 on the Wnt pathway (F). Results are shown from three independent experiments.
Figure 4.
Continued.
The authors apologize for these errors and advise they do not affect the results of the paper.