◀ Back to PTGS2

KDR — PTGS2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: KDR → PTGS2 (increases, PTGS2 Activity)
  Evidence: Nicotine has been also found to upregulate the vascular endothelial growth factor receptor (VEGFR) in gastric carcinoma cells by stimulating the expression of COX-2. This stimulation of COX-2 triggers tumor cell invasion and angiogenesis through activation of VEGFR-2, which subsequently modulates matrix metalloprotease activity (MMP2 and MMP9) and the expression of plasminogen activators [33].

Text-mined interactions from Literome

Rodrigues et al., FASEB J 2003 : Stimulation of angiogenesis by pS2 in the CAM assay is blocked by pharmacological inhibitors of cyclooxygenase COX-2 ( NS-398 ) and epidermal growth factor receptor (EGF-R) tyrosine kinase ( ZD1839 ), but is independent of KDR/Flk-1 and thromboxane A2 receptors
Yao et al., J Exp Clin Cancer Res 2011 (Neoplasms, Experimental...) : The results of RT-PCR and western blot showed that down-regulation of COX-2 might inhibit VEGF, Flt-1, Flk-1/KDR , angiopoietin-1, tie-2, MMP2 and OPN
Garonna et al., PloS one 2011 : Inhibition of VEGFR2 tyrosine kinase activity reduced leptin stimulated p38 ( MAPK ) and Akt activation, COX-2 induction, and pro-angiogenic EC responses, and blockade of VEGFR2 or COX-2 activities abolished leptin-driven neo-angiogenesis in a chick chorioallantoic membrane vascularisation assay in vivo