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MicroRNAs (miRs) have been demonstrated to be important regulators of malignant behavior in nasopharyngeal carcinoma (NPC) tumorigenesis. The present study aimed to investigate the biological roles and underlying mechanisms of miR-379 in NPC. The study initially observed that miR-379 was significantly downregulated in NPC clinical tissues and cell lines using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Next, gain-of-function assays were performed on human the NPC cell lines, C666-1 and 5-8F, including MTT, colony formation and transwell migration assays. The results indicated that ectopic expression of miR-379 suppressed the NPC cell proliferation, colony formation, migration and invasion in vitro . In addition, tumor protein D52 (TPD52) was identified as a direct target of miR-379 by a dual-luciferase reporter assay, while overexpression of miR-379 markedly reduced TPD52 expression at the mRNA and protein levels, as determined by RT-qPCR and western blot analysis, respectively. Furthermore, silencing of TPD52 significantly inhibited the C666-1 cell proliferation, migration and invasion. These findings suggest that miR-379 negatively regulates the growth and migration of NPC cells by downregulating TPD52 expression, while modulation of miR-379 expression may be a therapeutic strategy for NPC.

MicroRNA‑379 suppresses cell proliferation, migration and invasion in nasopharyngeal carcinoma by targeting tumor protein D52