MicroRNA-137 (miR-137) plays an important role in the development and 
progression of many types of human cancers; however, the role of miR-137 in 
retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the 
functional significance and molecular mechanisms of miR-137 in RB. We reported 
that miR-137 was frequently down-regulated in RB tissues and cell lines. The 
overexpression of miR-137 inhibited RB cell proliferation and invasion, while 
the suppression of miR-137 promoted RB cell proliferation and invasion. 
Bioinformatic analysis predicted that cyclooxygenase-2 (COX-2) was a potential 
target gene of miR-137, which was validated by a dual-luciferase reporter assay. 
Moreover, our results showed that miR-137 negatively regulated the expression of 
COX-2 and the production of prostaglandin E2 (PGE2) in RB cells. The knockdown 
of COX-2 suppressed the proliferation and invasion of RB cells as well as the 
production of PGE2. The overexpression of COX-2 significantly reversed the 
inhibitory effect of miR-137 overexpression on RB cell proliferation and 
invasion. Taken together, these results suggest that miR-137 suppresses the 
proliferation and invasion of RB cells by targeting COX-2/PGE2. Our study 
reveals a tumor suppressive role of miR-137 in the progression of RB and 
suggests miR-137 as a potentially effective therapeutic target for the treatment 
of RB.