Objective: To investigate the effects of miR-30e-5p on the proliferation, invasion and migration of nasopharyngeal carcinoma (NPC) cells, as well as its underlying mechanism.
Patients and methods: We detected the expressions of miR-30e-5p in NPC tissues, adjacent normal tissues, NPC cells (5-8F cells) and control cells (293T cells) by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The target gene of miR-30e-5p was predicted by online software and ubiquitin-specific peptidase 22 (USP22) was screened out. Luciferase reporter gene assay was performed after NPC cells were co-transfected miR-30e-5p mimics or miR-30e-5p inhibitor and mutant-type or wild-type USP22, respectively. Expressions of miR-30e-5p and USP22 in 5-8F cells were detected by qRT-PCR and Western blotting. The proliferation of 5-8F cells was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, and the invasion and migration abilities were detected by transwell assay. The activation of the epithelial-mesenchymal transition (EMT) was analyzed by detecting expressions of EMT-associated proteins (E-cadherin and Vimentin) in NPC cells.
Results: Expression level of miR-30e-5p was remarkably reduced, while USP22 expression was elevated in NPC tissues and cells compared with the controls. Molecular mechanism analysis con-firmed that miR-30e-5p could negatively regulate mRNA and protein levels of USP22 by binding to its specific sequence of 3'UTR. Subsequent experiments showed that USP22 knockdown resulting from up-regulation of miR-30e-5p could inhibit proliferation, invasion, migration, and EMT in 5-8F cells.
Conclusions: MiR-30e-5p was lowly expressed in NPC by targeting USP22, suggesting that miR-30e-5p could be used as a potential therapeutic target for NPC.