Upregulation of microRNA1945p inhibits hypopharyngeal carcinoma cell proliferation, migration and invasion by targeting SMURF1 via the mTOR signaling pathway

Hypopharyngeal carcinoma (HPC) is an aggressive malignancy with the worst prognosis among all head and neck cancers. MicroRNAs (miRNAs) are involved in the development of many human cancers, and may function as oncogenes or tumor suppressors. The present study aimed to evaluate the effects of miRNA (miR)1945p on the proliferation and invasion of HPC cells and to identify the potential regulatory mechanism. First, miR1945p and Smad ubiquitin regulatory factor 1 (SMURF1) expression levels were examined in HPC tissues. Subsequently, to explore the effects of miR1945p on SMURF1, a dualluciferase reporter gene assay was performed to verify the target relationship. To define the role of miR1945p in HPC progression, miR1945p upregulation and depletion were used to evaluate its effects on cell viability, invasion and migration. SMURF1 silencing and rapamycin [an inhibitor of the mammalian target of rapamycin (mTOR) signaling pathway] treatment were also used to analyze the regulatory mechanism in HPC. Finally, tumor growth was assessed in xenografted tumors in nude mice. SMURF1 was demonstrated to be highly expressed, whereas miR1945p was poorly expressed in HPC tissues; SMURF1 was identified as a target gene of miR1945p. FaDu hypopharyngeal squamous cell carcinoma cells treated with miR1945p mimics exhibited decreased viability, invasion and migration. The results indicated that miR1945p may inactivate the mTOR signaling pathway by targeting SMURF1. In addition, the in vivo experiments further verified these regulatory effects. These data suggested that miR1945ptargeted SMURF1 inhibition may be involved in the disruption of HPC progression through the repression of the mTOR signaling pathway.