MicroRNA-326 inhibits cell proliferative capacity and invasiveness through inhibiting the expression of ETS1 in nasopharyngeal carcinoma.

This study aims to detect microRNA-326 expression in nasopharyngeal carcinoma (NPC) tissues and cell lines and to explore the potential mechanism of microRNA-326 inhibiting the proliferative capacity and invasiveness of NPC cells. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine microRNA-326 expression in 40 cases of NPC tissue samples and cell lines. Meanwhile, microRNA-326 mimics were transfected into NPC cells to up-regulate microRNA-326 level. Next, the influence of microRNA-326 mimics on the proliferation and invasiveness of NPC cells was observed by Cell Counting Kit-8 (CCK-8) assay and transwell assay, respectively. Bioinformatics analysis was applied to search for target genes which may have direct effects on microRNA-326. An EST1 luciferase reporter vector containing microRNA-326 binding site was constructed and the binding relation between ETS1 and microRNA-326 was detected by Dual-Luciferase reporting assay. Lastly, the underlying mechanism of microRNA-326 and ETS1 in NPC was further verified via cell reverse experiments. Compared with control group, microRNA-326 expression was found remarkably decreased both in NPC tissue specimens and cell lines. The low expression of microRNA-326 could predict poor prognosis of patients with NPC. In vitro cell experiments revealed that overexpression of microRNA-326 remarkably inhibited the proliferative capacity and invasiveness of NPC cells. Bioinformatics analysis and Dual-Luciferase assay results suggested that microRNA-326 may bind to ETS1. Cell reverse assay indicated that inhibiting ETS1 expression partially reversed the changes in cell biological behavior induced by the down-regulation of microRNA-326 in CNE1 and 5-8F cell lines. Overexpression of microRNA-326 in NPC cells could remarkably inhibit the proliferative capacity and invasiveness of NPC cells. In addition, microRNA-326 may participate in the development of NPC by inhibiting ETS1 expression.