Gene expression profiling of pancreatic cancer cell line BxPC-3 induced by PAR-2 AP

  • Li Hsun Chang (Contributor)
  • Shiow-Lin Pan (Contributor)
  • Chin Yu Lai (Contributor)
  • An Chi Tsai (Contributor)
  • Che Ming Teng (Contributor)



Accession Number: GSE44827

GPL13693: Phalanx Human OneArray® v5

Organism: Homo sapiens

Published on 2013-04-30

Protease-activated receptor-2 (PAR-2), a G protein-coupled receptor activated by trypsin and coagulant factors, plays broad spectrum of physiological and pathological roles especially in cancer development. In this study, we used PAR-2 activating peptide to mimic the action of trypsin to trigger PAR-2 signaling pathway and effects of PAR-2 activation on gene expression in human pancreatic cancer cell line BxPC-3 investigated by microarray analysis. Through DAVID bioinformatic resources, we observed that activated PAR-2-mediated genes are summarized to two different pathways, renal cell carcinoma and NFkB pathway. In renal cell carcinoma pathway, activated PAR-2 dysregulated hypoxia-inducible factors and its target genes, including glucose transporter 1 (GLUT1), transforming growth factor-b (TGF-b) and vascular endothelial growth factor-A (VEGF-A). In addition, activated PAR-2 induced MAPK signaling and transcriptional factors, such as JUN, MAP2K1 and ETS1. The regulation of these genes by PAR-2 assumed that PAR-2 signaling was associated with cancer progression. On the other hand, activated PAR-2 upregulated interleukin-1b (IL-1b) and toll-like receptor 4 (TLR4) related with NFkB activation, which indicated that PAR-2 signaling may cause cancer-related inflammation. In conclusion, PAR-2 may be a factor to regulate cancer progression and inflammation.

Overall Design:
Two-condition experiment, control cells vs PAR-2 AP-treated cells.

Name: Che-Ming Teng
Organization: National Taiwan University
Deparment: Pharmacology
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