A tumor-suppressive microRNA, miR-504, inhibits cell proliferation and promotes apoptosis by targeting FOXP1 in human glioma

• MiR-504 downregulation correlated with aggressive clinicopathological features and poor survival in glioma patients.
• MiR-504 suppresses glioma tumorigenicity both in vitro and in vivo.
• MiR-504 regulated glioma tumorigenesis by downregulating expression of its direct target, FOXP1.
• MiR-504 might function as an important tumor suppressor of glioma tumorigenesis.

MicroRNAs (miRNAs) have been proposed as useful prognostic cancer biomarkers and as potential molecular targets for treating various cancers. Previous findings have indicated that miR-504 is dysregulated and involved in tumorigenesis of several types of cancer. However, the biological role of miR-504 in glioma remains unclear. In this study, we showed that miR-504 expression was markedly decreased in both glioma tissues and cell lines and that miR-504 downregulation significantly correlated with aggressive clinicopathological features and poor prognosis for glioma patients. In addition, miR-504 overexpression inhibited cell proliferation, induced cell cycle arrest, and promoted apoptosis in glioma cell lines. Furthermore, we identified forkhead box protein P1 (FOXP1) as a direct target of miR-504 using microarray analysis and a luciferase assay. Moreover, we demonstrated that miR-504 regulated glioma tumorigenesis by downregulating FOXP1 expression. Our results suggest that miR-504 might function as an important suppressor of glioma tumorigenesis and could serve as a promising candidate for therapeutic applications in glioma treatment.