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Fig. 5 | Molecular Cancer

Fig. 5

From: Overexpression of G protein-coupled receptor GPR87 promotes pancreatic cancer aggressiveness and activates NF-κB signaling pathway

Fig. 5

GPR87 up-regulation activates the NF-κB signaling pathway in pancreatic cancer. a. GSEA plots, demonstrating a significant correlation between the GPR87 mRNA expression levels in pancreatic cancer and the NF-κB-activated gene signatures from published datasets. b. Analysis of luciferase reporter activity in the indicated cells following transfection with 100 ng pNF-κB-luc plasmids or control-luciferase plasmid. c. Real-time PCR analysis demonstrating an apparent overlap between NF-κB-dependent gene expression and GPR87-regulated gene expression. The pseudo color represents an intensity scale for GPR87 versus vector or GPR87 siRNA versus control siRNA, calculated by log2 transformation. d. Western blotting analysis of the expression levels of the indicated proteins in the indicated cells. α-tubulin was used as a loading control. e. Quantification of colony numbers as determined by anchorage-independent growth assay. Colonies larger than 0.1 mm in diameter were scored. f. Quantification of tubule formation by HUVECs cultured in matrigel-coated plates with conditioned media from pancreatic cancer cells transfected with the vector, IκBα-mut or treated with the NF-κB inhibitor (JSH-23). g. Quantification of gemcitabine-induced (1 μM) TUNEL-positive cells in pancreatic cells transfected with vector, IκBα-mut or treated with the NF-κB inhibitor. Each bar represents the mean ± SD of three independent experiments. *p < 0.05

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