Fig. 3
From: Identification of GRIN2D as a novel therapeutic target in pancreatic ductal adenocarcinoma
GRIN2D promotes PDAC progression by CREB/ p38 MAPK signaling pathway. (A). p38, MSK, and CREB were dephosphorylated after knockdown of GRIN2D in SW1990 and PANC04.03 cells. (B). Clinical correlation between GRIN2D and p-CREB levels in PDAC primary tumors. (C). Amount of common differential genes in SW1990 and PANC04.03 cells after knockdown of GRIN2D. (D). Expression of differential genes after knockdown of GRIN2D. (E). Correlation between GRIN2D and IL20RB, CCL22, G5S2, IL6, EPGN, and HMGA2 expression in PDAC tumors. (F). IL20RB, CCL22, G5S2, IL6, EPGN, and HMGA2 expression in tumor and non- tumor groups from two independent samples cohort GSE16515 and GSE15471. (G). Survival analysis of IL20RB, CCL22, G5S2, IL6, EPGN, and HMGA2 in PDAC patients. (H). Phosphorylated CREB binding to HMGA2 and IL20RB in SW1990 and PANC04.03 cells, as revealed by ChIP assay. (I). EMT markers ZEB1, SNAIL, SLUG, and TWIST were downregulated after knockdown of GRIN2D in SW1990 and PANC04.03 cells. Data are from at least three independent experiments. Mean ± SD. *, P < 0.05; **, P < 0.01; ***, P < 0.001