Cyclooxgenase-2 (COX-2) knock-out mouse experiments showed that COX-2 was 
necessary for in vivo allergic inflammation, such as passive cutaneous 
anaphylaxis, passive systemic anaphylaxis, and triphasic cutaneous allergic 
reaction. TargetScan analysis predicted COX-2 as a target of miR-26a and 
miR-26b. miR-26a/-26b decreased luciferase activity associated with 
COX-2-3'-UTR. miR-26a/-26b exerted negative effects on the features of in vitro 
and in vivo allergic inflammation by targeting COX-2. ChIP assays showed the 
binding of HDAC3 and SNAIL, but not COX-2, to the promoter sequences of miR-26a 
and miR-26b. Cytokine array analysis showed that the induction of chemokines, 
such as MIP-2, in the mouse passive systemic anaphylaxis model occurred in a 
COX-2-dependent manner. ChIP assays showed the binding of HDAC3 and COX-2 to the 
promoter sequences of MIP-2. In vitro and in vivo allergic inflammation was 
accompanied by the increased expression of MIP-2. miR-26a/-26b negatively 
regulated the expression of MIP-2. Allergic inflammation enhanced the 
tumorigenic and metastatic potential of cancer cells and induced positive 
feedback involving cancer cells and stromal cells, such as mast cells, 
macrophages, and endothelial cells. miR-26a mimic and miR-26b mimic negatively 
regulated the positive feedback between cancer cells and stromal cells and the 
positive feedback among stromal cells. miR-26a/-26b negatively regulated the 
enhanced tumorigenic potential by allergic inflammation. COX-2 was necessary for 
the enhanced metastatic potential of cancer cells by allergic inflammation. 
Taken together, our results indicate that the miR26a/-26b-COX-2-MIP-2 loop 
regulates allergic inflammation and the feedback relationship between allergic 
inflammation and the enhanced tumorigenic and metastatic potential.