Journal: Journal of cell communication and signaling
Article Title: Mutant p53 gain-of-function stimulates canonical Wnt signaling via PI3K/AKT pathway in colon cancer.
doi: 10.1007/s12079-023-00793-4
Figure Lengend Snippet: Fig. 3 Mutant p53 knockdown in the SW480 cell line decreases canonical Wnt pathway. A Comparation of non-phospho- rylated β-catenin (active) and p53 protein levels measured in different colon cancer cell lines with different TP53 status, RKO (wild-type p53), SW480 (R273H p53), and SW620 (R273H p53). Densitometric analysis of immunoblots of p53 and active β-catenin was performed using GAPDH as a loading control. B Representa- tive immunoblots and graph of p53 protein in SW480 under different doses of siRNA p53 (25–100 nM); the scramble condition was used as a control (100 nM). C Luciferase activity measured with the TOP/FOP system in both scramble and siRNA p53 (100 nM) condi- tions. The relative units were normalized to Renilla activity. D Representative immunoblot and graph of c-myc normalized to GAPDH. E. Representa- tive colonies and relative area quantification corresponding to scramble and shp53 conditions of SW480-transduced cells. Graphs represent densito- metric analysis from at least three independent experiments (means ± SEM). *p < 0.05, **p < 0.01, ***p < 0.001
Article Snippet: The PI3K/AKT inhibitor wortmannin was obtained from Sigma (Cat. No. 19545-26-7), and the p53 Activator III compound RITA was from Santa Cruz Biotechnology (Cat. No. sc-202743).
Techniques: Mutagenesis, Knockdown, Western Blot, Control, Luciferase, Activity Assay