Oral squamous cell carcinoma (OSCC) is the most commonly diagnosed oral cavity malignancy. A handful of circular RNAs (circRNAs) have recently shown to act as crucial regulators in OSCC, including circRNA plasmacytoma variant translocation 1 (circ-PVT1). However, further exploration is still needed for the underlying functional mechanism behind circ-PVT1 in OSCC. The levels of circ-PVT1, microRNA-106a-5p (miR-106a-5p) and hexokinase II (HK2) were all examined applying with quantitative real-time polymerase chain reaction (qRT-PCR). Cellular analyses (cell viability, apoptosis, metastasis and glycolysis) in vitro were performed via cell counting kit-8 (CCK-8), flow cytometry, transwell migration/invasion assays and glycolysis-related indications (glucose consumption, lactate production and ATP/ADP ratio). HK2 protein level was measured through western blot. Dual-luciferase reporter assay was conducted to study the interplay between miR-106a-5p and circ-PVT1 or HK2. Xenografts in mice were used for analyzing circ-PVT1 in vivo. Circ-PVT1 was expressed with abnormal high level while miR-106a-5p was down-regulated in OSCC tissues and cells. Circ-PVT1 knockdown reduced OSCC cell growth, metastasis and glycolysis. Moreover, circ-PVT1 acted in OSCC by functioning as a miR-106a-5p sponge. HK2 was a target of miR-106a-5p and miR-106a-5p played an anti-tumor role in OSCC by inhibiting HK2. Furthermore, HK2 could be regulated by circ-PVT1 via targeting miR-106a-5p. In xenograft models of mice, down-regulation of circ-PVT1 retarded tumorigenesis via the miR-106a-5p/HK2 axis. Our works suggested that circ-PVT1 directly combined with miR-106a-5p to mediate HK2 level, consequently regulating cellular behaviors in OSCC as a tumor promoter.

口腔鳞状细胞癌（OSCC）是最常见的口腔恶性肿瘤。最近显示，少数环状RNA（circRNA）在OSCC中起着至关重要的调节作用，包括circRNA浆细胞瘤变体易位1（circ-PVT1）。但是，仍需要对OSCC中circ-PVT1背后的潜在功能机制进行进一步的探索。应用定量实时聚合酶链反应（qRT-PCR）检测了circ-PVT1，microRNA-106a-5p（miR-106a-5p）和己糖激酶II（HK2）的水平。通过细胞计数试剂盒8（CCK-8），流式细胞仪，transwell迁移/侵袭测定和糖酵解相关的适应症（葡萄糖消耗，乳酸产生和ATP /），进行了体外细胞分析（细胞活力，凋亡，转移和糖酵解） ADP比率）。HK2蛋白水平通过蛋白质印迹法测量。进行了双重荧光素酶报告基因分析，以研究miR-106a-5p与circ-PVT1或HK2之间的相互作用。小鼠体内的异种移植物用于体内分析circ-PVT1。Circ-PVT1在OSCC组织和细胞中异常高水平表达，而miR-106a-5p被下调。Circ-PVT1抑制可减少OSCC细胞的生长，转移和糖酵解。此外，circ-PVT1通过充当miR-106a-5p海绵在OSCC中起作用。HK2是miR-106a-5p的靶标，而miR-106a-5p通过抑制HK2在OSCC中发挥抗肿瘤作用。此外，HK2可以由circ-PVT1通过靶向miR-106a-5p调控。在小鼠异种移植模型中，circ-PVT1的下调通过miR-106a-5p / HK2轴抑制了肿瘤发生。