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. 2022 Dec 10;12(12):e1126. doi: 10.1002/ctm2.1126

FIGURE 6.

FIGURE 6

CSTB is up‐regulated by SP1 in pancreatic ductal adenocarcinoma (PDAC). (A) Predicted H3K27ac binding site in CSTB promoter from UCSC genome browser. Real‐time expression of CSTB in CFPAC and Patu 8988 treated with DMSO, A485 or C646 in RNA (B) and protein (C) levels. (D) Diagram showing the designed corresponding primers. (E) Heatmap showing relative H3K27ac reads in five segments of CSTB promoter in nine cell lines. (F) Average H3K27ac reads of CSTB promoter in eight PDAC cell lines, relative to HPNE. (G) Venn diagram showing TF screening strategy. (H) Analysis of correlation between CSTB and SP1 (left) and TFAP2A (right) in TCGA. Real‐time expression of CSTB in CFPAC and Patu 8988 transfected with si‐SP1 or si‐TFAP2A in RNA (I) and protein (J) levels. (K) The sequence logo graph manifested the canonical binding site of SP1 predicted by JASPAR. (L) Luciferase activity in HEK‐293T cells co‐transfected with SP1 or scramble sequence and plasmid. (M) Two representative IHC staining images of SP1 and CSTB in Ruijin TMA. (N) Correlation between CSTB and SP1 in Ruijin TMA. (O) Respective sample counts in tumour tissues and adjacent tissues. (P) Kaplan–Meier analysis of overall survival rate related to the expression of SP1 in Ruijin TMA *p < .05, **p < .01, ***p < .001, and ****p < .0001