miR-4792 inhibits epithelial–mesenchymal transition and invasion in nasopharyngeal carcinoma by targeting FOXC1

• DOI: 10.1016/j.bbrc.2015.11.045
• Publication Date: 2015-11-14T13:00:37Z
• Authors: Ying Li; Xiangdong Chen
• Keywords: Gene Expression Regulation, Neoplastic; 0301 basic medicine; MicroRNAs; 03 medical and health sciences; Epithelial-Mesenchymal Transition; Cell Line, Tumor; Humans; Forkhead Transcription Factors; Nasopharyngeal Neoplasms; Neoplasm Invasiveness; Protein Binding

Through analysis of a published micro-array-based high-throughput assessment, we discovered that miR-4792 was markedly down-regulated in nasopharyngeal carcinoma (NPC) tissues. However, little is known about its effect and mechanism involved in NPC development and progression. Here, we reported the role of miR-4792 in epithelial-mesenchymal transition (EMT) and invasion in NPC. We identified an inverse correlation between miR-4792 expression level and NPC cell EMT and invasion, and up-regulation of miR-4792 inhibited NPC cell EMT and invasion. Moreover, we identified and validated that FOXC1 was a direct target of miR-4792, and miR-4792 regulated EMT and invasion in NPC by acting directly on the 3'UTR of FOXC1 mRNA. We also performed the animal experiments to explore the anti-tumor effect of miR-4792, and found that overexpression of miR-4792 inhibited the growth of nasopharyngeal tumors in vivo. These findings suggest that miR-4792 functions as a tumor suppressor in NPC development and progression by targeting FOXC1, which could act as a novel potential therapeutic target for NPC treatment, and miR-4792/FOXC1 pathway that we studied might be used for NPC treatment in future.