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Background  As a distinctive type of head and neck cancers, nasopharyngeal carcinoma (NPC) is genesis from the clonal Epstein-Barr virus (EBV)-infected nasopharyngeal epithelial cells accumulated with multiple genetic lesions. Among the recurrent genetic alterations defined, loss of 9p21.3 is the most frequent early event in the tumorigenesis of EBV-associated NPC. In addition to the reported  CDKN2A/p16 , herein, we elucidated the role of a miRNA,  miR-31  within this 9p21.3 region as NPC-associated tumor suppressor.    Methods  The expression and promoter methylation of miR-31 were assessed in a panel of NPC tumor lines and primary tumors. Its  in vitro  and  in vivo  tumor suppression function was investigated through the ectopic expression of  miR-31  in NPC cells. We also determined the  miR-31  targeted genes and its involvement in the growth in NPC.    Results  Downregulation of  miR-31  expression was detected in almost all NPC cell line, patient-derived xenografts (PDXs) and primary tumors. Both homozygous deletion and promoter hypermethylation were shown to be major mechanisms for  miR-31  silencing in this cancer. Strikingly, loss of  miR-31  was also obviously observed in the dysplastic lesions of nasopharynx. Restoration of  miR-31  in C666-1 cells inhibited the cell proliferation, colony-forming and migratory capacities. Dramatic reduction of  in v itro anchorage-independent growth and  in vivo  tumorigenic potential were demonstrated in the stable clones expressing  miR-31 . Furthermore, we proved that  miR-31  suppressed the NPC cell growth via targeting FIH1 and MCM2.    Conclusions  The findings provide strong evidence to support  miR-31  as a new NPC-associated tumor suppressor on 9p21.3 region. The inactivation of  miR-31  may contribute to the early development of NPC.

miR-31 is consistently inactivated in EBV-associated nasopharyngeal carcinoma and contributes to its tumorigenesis