Gene interactions and pathways from curated databases and text-mining

◀ Back to IGF2

IGF2 — PTGS2

Text-mined interactions from Literome

Di Popolo et al., Oncogene 2000 (Disease Progression...) : Up-regulation of COX-2 expression by IGF-II is mediated through activation of IGF-I receptor because: (i) treatment of Caco-2 cells with a blocking antibody to the IGF-I receptor inhibits COX-2 mRNA expression ; ( ii ) transfection of Caco-2 cells with a dominant negative IGF-I receptor reduces COX-2 expression and activity ... Also, the blockade of the PI3-kinase, that mediates the proliferative effect of IGF-I receptor in Caco-2 cells, inhibits IGF-II dependent COX-2 up-regulation and PGE2 synthesis
Kim et al., J Invest Dermatol 2004 (MAP Kinase Signaling System) : IGF-II mediated COX-2 gene expression in human keratinocytes through extracellular signal regulated kinase pathway ... IGF-II induced COX-2 mRNA and protein levels, and the up-regulation of COX-2 expression by IGF-II was reduced by pretreatment with inhibitors of tyrosine kinase, Src and PI3-kinase ... To further examine the roles of these mitogen activated protein kinases ( MAPKs ) in IGF-II induced COX-2 expression, we performed COX-2 promoter analysis using dominant negative plasmids of MEK1 ( DN-MEK1 ), p38 ( DN-p38 ) and JNK1 ( DN-JNK1 ) ... Although IGF-II increased COX-2 promoter activity approximately 2.5-fold, this increase was blocked by cotransfection with DN-MEK1 or DN-JNK1 ... However, DN-p38 did not block the IGF-II induced COX-2 promoter activity ... These results suggest that IGF-II induces COX-2 expression through the tyrosine kinase-Src-ERK and tyrosine kinase-PI3-kinase pathways, but not via p38 MAPK pathway, and that the basal JNK activity is required for the upregulation of COX-2 by IGF-II, as well
Stoeltzing et al., Cancer Lett 2007 (Pancreatic Neoplasms) : Regulation of cyclooxygenase-2 (COX-2) expression in human pancreatic carcinoma cells by the insulin-like growth factor-I receptor ( IGF-IR ) system ... We hypothesized that IGF-IR is directly involved in induction of COX-2 and sought to investigate signaling pathways mediating this effect