循环RNA（circRNA）已被确认为细胞生理过程的潜在功能调节因子。本研究旨在了解hsa_circ_0005050（circ_0005050）在口腔鳞状细胞癌（OSCC）中的潜在分子机制。采用定量逆转录-聚合酶链反应（qRT-PCR）检测circ_0005050、miR-487a-3p和软骨糖胺硫酸化酶1（CHSY1）的表达情况。采用双荧光素酶报告系统、RNA pull-down和RNA免疫共沉淀（RIP）实验确定miR-487a-3p与circ_0005050或CHSY1之间的结合关系。采用集落形成实验和EdU实验研究增殖。采用划痕愈合和Transwell实验检测细胞迁移。流式细胞术检测OSCC细胞的凋亡率。 Western blot确定相关因子的蛋白水平。建立肿瘤异种移植模型以确定circ_0005050在体内对肿瘤生长的调节作用，并使用免疫组织化学（IHC）检测该异种移植物中的Ki-67表达。我们发现，在OSCC组织细胞中，circ_0005050显然上调。在功能实验中，抑制circ_0005050明显减缓了体外的OSCC生长。此外，我们进行了双荧光素酶报告实验和RNA pull-down实验，以验证circ_0005050促进了miR-487a-3p。抑制miR-487a-3p复苏了由circ_0005050敲低引起的SCC15和SCC25细胞增殖抑制。此外，我们发现CHSY1的过表达也逆转了circ_0005050沉默对细胞增殖的抑制作用。此外，circ_0005050敲低抑制了体内肿瘤生长。circ_0005050通过miR-487a-3p / CHSY1轴在OSCC进展中作为一个致癌因子。 ©2022中国牙科科学联合会。由Elsevier B.V.提供的出版服务。

Circular RNAs (circRNAs) have been identified as potential functional modulators of the cellular physiology processes. This study aims to learn the potential molecular mechanisms of hsa_circ_0005050 (circ_0005050) in oral squamous cell carcinoma (OSCC).Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to examine the expression of circ_0005050, miR-487a-3p, and chondroitin sulfate synthase 1 (CHSY1). Dual-luciferase reporter system, RNA pull-down, and RNA Immunoprecipitation (RIP) assays were used to determine the binding between miR-487a-3p and circ_0005050 or CHSY1. Colony formation experiment and EdU assay were used to investigate proliferation. Wound-healing and transwell assays were used to detect the migration of cells. The apoptosis rate of OSCC cells was tested by flow cytometry. Protein levels of related factors were determined by Western blot. Tumor xenograft was established to determine the regulatory role of circ_0005050 on tumor growth in vivo, and Ki-67 expression was detected in this xenograft using Immunohistochemical (IHC).We implicated that circ_0005050 was apparently upregulated in OSCC tissues cells. In function experiments, repressing of circ_0005050 remarkably retarded OSCC growth in vitro. Furthermore, we conducted dual-luciferase reporter assays and RNA pull-down assays to verify that circ_0005050 sponged miR-487a-3p. Suppression of miR-487a-3p rescued the inhibition of proliferation in SCC15 and SCC25 cells induced by circ_0005050 knockdown. In addition, we found that overexpression of CHSY1 also reversed the inhibitory effect of circ_0005050 silencing on cell proliferation. Moreover, circ_0005050 knockdown inhibited tumor growth in vivo.Circ_0005050 acted as an oncogenic factor in OSCC progression through miR-487a-3p/CHSY1 axis.© 2022 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V.