Silencing of <i>PTGR2</i> suppressed growth rates of pancreatic cancer cells capable of self-producing abundant prostaglandins.

<p><b>(A)</b> Western blot analysis of expression levels of COX1, COX2, 15-PGDH, and PTGR2 in PL45, PANC-1, MIA PaCa-2, BxPC-3, and Capan-2 cells. Hsp70 served as a loading control. <b>(B</b> and <b>C</b>) Relative levels of intracellular <b>(B)</b> 15-keto-PGE₂ and <b>(C)</b> 13,14-dihydro-15keto-PGE₂ isolated from various pancreatic cancer cell lines. The concentrations of 15-keto-PGE₂ and 13,14-dihydro-15keto-PGE₂ extracted from BxPC-3 were set as 1, and the relative levels of 15-keto-PGE₂ and 13,14-dihydro-15-keto-PGE₂ from other cell lines were presented as values relative to BxPC-3 cells. Prostaglandins were isolated and analyzed by LC-MS/MS. The results are the average of 4 independent experiments. <b>(D)</b> Efficiency of siRNA-mediated <i>PTGR2</i> silencing. PTGR2 protein expression in PL45, PANC-1, MIA PaCa-2, BxPC-3 and Capan-2 cells was detected by Western blot analysis. Hsp70 served as a loading control. Time indicated hours post-siRNA transfection. <b>(E</b>–<b>I</b>) Relative proliferation rates of <b>(E)</b> PL45 <b>(F)</b> PANC-1 <b>(G)</b> MIA PaCa-2 <b>(H)</b> BxPC-3 and <b>(I)</b> Capan-2 si-PTGR2 cells as compared to si-Control cells. Cell proliferation was evaluated by MTS assay at the indicated time points. 48 hours post-transfection was set as Day 1. The values were obtained from 2 independent experiments each done in triplicate. Data are presented as the mean ± SE. * P < 0.05, Student’s t-test.