Emerging evidence has demonstrated the pivotal roles of circular RNAs (circRNAs) in the modulation of malignancy and pathological progression among multiple human cancers. Glucose metabolism reprogramming is a widely identified characteristic for contributing to facilitate tumorigenesis. Nonetheless, their contributions to head and neck squamous cell carcinoma (HNSCC) cell glycolysis remain to be further elucidated. Herein, we aim to investigate the role of circRNA, hsa_circ_0018180 (also named as circPARD3) in HNSCC. Expression patterns of circPARD3 in HNSCC tissues and different cell lines were determined by qRT-PCR assay, as well as its correlation with the prognosis of survival. CCK-8, EdU incorporation, and transwell assays were carried out to assess the cell viability, proliferation, migration, and invasion, respectively. Glucose uptake and lactate production were evaluated by preforming glycolysis. Mechanistically, the circPARD3/miR-5194/ENO1 axis was verified by RNA immunoprecipitation (RIP) and luciferase reporter assays. Western blot analysis was employed to measure the epithelial-mesenchymal transition (EMT)-associated biomarkers. Upregulated circPARD3 observed in HNSCC tissues and cell lines indicated the poor prognosis of patients. Stable knockdown of circPARD3 dramatically exerted the suppressive effects on cell viability, proliferation, migration, and invasion, as well as glucose uptake and lactate production. Mechanistically, circPARD3 harbored miR-5194, serving as a miRNA sponge, thereby increasing ENO1 expression. Moreover, ENO1 evidently reversed miR-5194-mediated attenuated malignant behaviors. Collectively, our study identified an oncogenic role of circPARD3 in HNSCC through a novel machinery of circPARD3/miR-5194/ENO1 and provided a promising therapeutic target for HNSCC.

新出现的证据表明，环状 RNA (circRNA) 在调节多种人类癌症的恶性肿瘤和病理进展中起着关键作用。葡萄糖代谢重编程是一种广泛识别的有助于促进肿瘤发生的特征。尽管如此，它们对头颈部鳞状细胞癌 (HNSCC) 细胞糖酵解的贡献仍有待进一步阐明。在此，我们旨在研究 circRNA hsa_circ_0018180（也称为 circPARD3）在 HNSCC 中的作用。通过 qRT-PCR 测定 circPARD3 在 HNSCC 组织和不同细胞系中的表达模式，及其与生存预后的相关性。进行 CCK-8、EdU 掺入和 transwell 测定，以分别评估细胞活力、增殖、迁移和侵袭。通过预形成糖酵解评估葡萄糖摄取和乳酸生成。从机制上讲，circPARD3/miR-5194/ENO1 轴通过 RNA 免疫沉淀 (RIP) 和荧光素酶报告基因检测得到验证。采用蛋白质印迹分析来测量上皮-间质转化 (EMT) 相关生物标志物。在 HNSCC 组织和细胞系中观察到上调的 circPARD3 表明患者预后不良。稳定敲低 circPARD3 可显着抑制细胞活力、增殖、迁移和侵袭，以及葡萄糖摄取和乳酸产生。从机制上讲，circPARD3 含有 miR-5194，充当 miRNA 海绵，从而增加 ENO1 的表达。此外，ENO1 明显逆转了 miR-5194 介导的减弱的恶性行为。总的来说，