Abstract: Objective To investigate the impact of the miR-106a-5p/programmed death-ligand 1 (PD-L1) axis on the malignant biological behavior of nasopharyngeal carcinoma (NPC) cells and its molecular mechanism. 
Methods The expression levels of miR-106a-5p and PD-L1 mRNA in the NPC cell line HNE1 and immortalized normal nasopharyngeal epithelial cell line NP69 were measured using quantitative real-time PCR (RT-qPCR), and PD-L1 protein expression was assessed by Western blotting. A dual-luciferase reporter assay was performed to verify the direct regulatory relationship between miR-106a-5p and PD-L1. HNE1 cells were transfected with miR-106a-5p mimics, inhibitors, si-PD-L1, or PD-L1 overexpression plasmids. Cell proliferation was evaluated by the CCK-8 assay, while cell migration and invasion were assessed using scratch assays and Transwell assays, respectively. 
Results The expression levels of miR-106a-5p and PD-L1 were significantly higher in NPC cells than in normal nasopharyngeal epithelial cells (miR-106a-5p: P=0.001，PD-L1-mRNA: P=0.012, PD-L1-protein: P=0.008). The dual-luciferase reporter assay confirmed that PD-L1 was a direct target of miR-106a-5p. miR-106a-5p significantly increased the mRNA and protein levels of PD-L1 (P=0.010; P=0.037), whereas the miR-106a-5p inhibitor markedly suppressed PD-L1 expression (P＜0.001). Overexpression of PD-L1 led to a significant upregulation of miR-106a-5p (P＜0.05), and knockdown of PD-L1 significantly reduced miR-106a-5p levels (P＜0.05). Overexpression of either miR-106a-5p or PD-L1 significantly enhanced the proliferation, invasion and migration of HNE1 cells (bothP＜0.05), while knockdown of either PD-L1 or miR-106a-5p reversed these effects (both P＜0.05). Conversely, knockdown of miR-106a-5p or PD-L1 significantly inhibited cell proliferation, invasion and migration, and overexpression of either PD-L1 or miR-106a-5p could reverse this inhibition (both P＜0.05). 
Conclusion There is a positive feedback regulation between miR-106a-5p and PD-L1, which promotes the proliferation, migration, and invasion of NPC cells.

Key words: nasopharyngeal carcinoma, cell proliferation, migration and invasion