MiR-92a regulates oral squamous cell carcinoma (OSCC) cell growth by targeting FOXP1 expression

Increasing evidence indicates that microRNAs dysregulation contributes to the development and progression of various human cancers, including oral squamous cell carcinoma (OSCC). However, little is known about the potential role of microRNA-92a (miR-92a) in OSCC. Thus, the aim of this study was to investigate the effects of miR-92a expression on OSCC cell growth, apoptosis and tumorigenesis. Real-time quantitative polymerase chain reaction was used to detect the expression level of miR-92a in primary tumor tissues and OSCC cell lines. The effects of miR-92a on cell proliferation, cell cycle, apoptosis and tumorigenesis of OSCC cells were explored after miR-92a expression was increased or decreased in the UM1 and Tca-8113 cells, respectively. The 3'-untranslated region (3'-UTR) of FOXP1 combined with miR-92a was analyzed with dual-luciferase reporter assays. The level of miR-92a expression was significantly up-regulated in the OSCC tissues and cell lines. The up-regulation of miR-92a expression promoted UM1 cell proliferation, cell cycle progression in vitro and tumor growth in nude mice, but its expression reduction inhibited these processes and induced apoptosis in Tca-8113 cells. Additionally, miR-92a expression was inversely correlated with FOXP1 protein expression in the OSCC tissues and cell lines. Furthermore, FOXP1 was identified as a functional downstream target of miR-92a by directly targeting the 3'-UTR of FOXP1. These findings indicate that miR-92a may act as a tumor inducer in OSCC by suppressing FOXP1 expression, and it could serve as a potential therapeutic target for OSCC treatment.