Hsa_circ_0005050 regulated the progression of oral squamous cell carcinoma via miR-487a-3p/CHSY1 axis

Background/purpose: Circular RNAs (circRNAs) have been identified as potential functional modulators of the cellular physiology processes. This study aims to learn the poten-tial molecular mechanisms of hsa_circ_0005050 (circ_0005050) in oral squamous cell carcinoma (OSCC).Materials and methods: Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to examine the expression of circ_0005050, miR-487a-3p, and chondroitin sul-fate synthase 1 (CHSY1). Dual-luciferase reporter system, RNA pull-down, and RNA Immunopre-cipitation (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 regula-tory role of circ_0005050 on tumor growth in vivo, and Ki-67 expression was detected in this xenograft using Immunohistochemical (IHC).Results: 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.Conclusion: 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. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).