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MicroRNAs are short non-coding RNAs that regulate gene expression and are crucial to tumorigenesis. Oral squamous cell carcinoma (OSCC) is a prevalent malignancy worldwide. Up-regulation of  miR-146  has been identified in OSCC tissues. However, the roles of  miR-146  in carcinogenesis are controversial as it is suppressive in many other malignancies. The present study investigated the pathogenic implications of  miR-146a  in oral carcinogenesis. Microdissected OSCC exhibits higher levels of  miR-146a  expression than matched adjacent mucosal cells. The plasma  miR-146a  levels of patients are significantly higher than those of control subjects; these levels decrease drastically after tumor resection.  miR-146a  levels in tumors and in patients’ plasma can be used to classify OSCC and non-disease status (sensitivity: >0.72). Exogenous  miR-146a  expression is significantly increased  in vitro  oncogenic phenotypes as well as during xenograft tumorigenesis and OSCC metastasis. The plasma  miR-146a  levels of these mice parallel the xenograft tumor burdens of the mice. A  miR-146a  blocker abrogates the growth of xenograft tumors.  miR-146a  oncogenic activity is associated with down-regulation of IRAK1, TRAF6 and NUMB expression. Furthermore,  miR-146a  directly targets the 3′UTR of NUMB and a region within the NUMB coding sequence when suppressing NUMB expression. Exogenous NUMB expression attenuates OSCC oncogenicity. Double knockdown of IRAK1 and TRAF6, and of TRAF6 and NUMB, enhance the oncogenic phenotypes of OSCC cells. Oncogenic enhancement modulated by  miR-146a  expression is attenuated by exogenous IRAK1 or NUMB expression. This study shows that  miR-146a  expression contributes to oral carcinogenesis by targeting the IRAK1, TRAF6 and NUMB genes.

miR-146a Enhances the Oncogenicity of Oral Carcinoma by Concomitant Targeting of the IRAK1, TRAF6 and NUMB Genes