MiR-150, localized on chromosome 19q13, has been indicated as a hematopoietic-specific miRNA in malignant lymphoma and has been observed to be significantly downregulated in tumor cells relative to healthy cells. The abnormal expression of miR-150 has also been found in other various solid tumor tissues, such as lung cancer, gastric cancer, colorectal cancer, endometrial cancer, EOC, and pancreatic cancer. Especially, Vang et al. found that miR-150 displayed low expression in most primary EOC tissues; Shapira et al. also reported that miR-150 showed at least a 10-fold decrease in expression in pre-surgical plasma samples from women diagnosed with EOC compared with plasma samples from women without a known pelvic mass. These findings imply a possible role of miR-150 in human EOC, which prompted us to identify and functionally validate miR-150-associated clinical significance and molecular mechanisms in EOC. EOC is still a major Polygalasaponin-F gynecologic problem with low 5-year survival rate and seriously threatens human health due to distance metastases, despite routine surgery and chemotherapy. Growing evidence display the dysregulation of various miRNAs in EOC and imply their essential roles in tumorigenic processes, including cell proliferation, apoptosis and motility. Thus, revealing the molecular changes of miRNAs is crucial for overcoming this deadly disease. Previous studies have 3beta-acetoxy-eupha-7-25-dien-24(R)-ol demonstrated that miR-150 is dramatically downregulated in human EOC tissues and patients�� serum compared to normal controls. However, the roles of miR-150 in initiation and progression of EOC and the downregulation of miR-150 expression in this cancer are still unclear. In the current study, we linked miR-150 to its target gene ZEB1, and demonstrated their involvements in regulating malignant phenotypes of ovarian cancer cells. We confirmed the key role of miR150 as a tumor suppressor by directly and negatively targeting ZEB1 in EOC. The evidence for this comes from the following sources. First, we validated the downregulation of miR-150 in EOC tissues using a large cohort of EOC patients, and showed that low miR-150 expression level was much lower in highly aggressive EOC tissues.