Fig. 4
LPA produced by LIPH promoted PDAC progression through enhancing glycolysis. A GSEA using hallmark gene sets was performed to compare PANC-1 control and PANC-1 sh1-LIPH-transfected cells treated with PA (10 µM). NES, normalized enrichment score. B A heatmap showing the expression of the glycolysis-related genes and hypoxia-related genes in PANC-1 NC and LIPH-knockdown cells in the presence of PA (10 µM). C Relative mRNA levels of glycolysis-related genes of PDAC with or without LIPH inhibition in the presence of PA (10 µM) treatment. Expression was detected by q-PCR. D ECAR detected by Seahorse analyzer in control and sh1-LIPH-transfected cells (PANC-1 up, CFPAC-1 low). Cells were seeded and cultured one day in 0.5% FAF-BSA complete medium (starvation), and then exogenous PA (10 µM) or LPA (10 µM) was added to culture cell before analysis. E ATP production of PC cells with or without LIPH inhibition (Glc: Glucose; O: oligomycin; 2-DG: 2-deoxyglucose). F Graph of 18F-FDG uptake in the subcutaneous xenograft model. Control and sh1-LIPH-transfected CFPAC-1 cells were used to establish the subcutaneous xenograft. G Representative images of LIPH expression in tumor tissues from PDAC patients who received preoperative 18F-FDG PET/CT examination. The difference in SUVmax value between LIPHhigh patients and LIPHlow patients was further analyzed. Scale bar = 100 µm. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001