Abnormal angiogenesis is critically involved in tumor progression and metastasis 
including endometrial cancer and is regulated by microRNAs such as microRNA-101 
(miR-101). We hypothesize that miR-101 expression is disrupted in endometrial 
cancer and modulation of miR-101 levels is sufficient to regulate tumor growth 
through angiogenesis. We examined the expression levels of miR-101 and factors 
involved in angiogenesis in the patients with endometrial cancer. We also 
overexpressed or inhibited miR-101 in RL-95-2 cells and examined their effects 
on cell toxicity and tumor growth. Finally, we determined if miR-101 regulated 
tumorigenesis through cyclooxygenase-2 (COX-2). We found that miR-101 levels 
were significantly reduced. Factors involved in angiogenesis included vascular 
endothelial growth factor-A (VEGF-A), thrombospondin-1 (TSP-1), cyclooxygenase-2 
(COX-2), prostaglandin E2 (PGE2), and aromatase (P450arom), which were increased 
in endometrial carcinoma. Modulation of miR-101 level was sufficient to affect 
tumor growth. Finally, we found that the effects of miR-101 inhibition on tumor 
growth were suppressed by COX-2 inhibition. Our results suggest that modulating 
miR-101 and COX-2 levels or their activity may be a potential therapeutic 
strategy for endometrial cancer.