Effects of interfering circ_0072088 on the biological behavior of nasopharyngeal carcinoma cells in vitro

LI Xinhua; LI Jun; PEI Zhuo

doi:10.3969/j.issn.1002-7386.2025.09.007

Abstract：Objective To investigate the effects of interfering circular RNA 0072088(circ_0072088)on the biological behavior of nasopharyngeal carcinoma cells and its possible mechanism.Methods The relative levels of circ_0072088 and microRNA(miR)-223 in the serum of patients with nasopharyngeal carcinoma and healthy subjects were detected by Real-time quantitative PCR(RT-qPCR).The nasopharyngeal carcinoma C666-1 cells were divided into control group,short interfering RNA negative control(si NC)group and circ_0072088 short interfering RNA(si-circ_0072088)group.Thiazole blue method and colony formation test were applied to examine the proliferation of C666-1 cells.Flow cytometry was used to detect the apoptosis rate of C666-1 cells.Moreover,scratch healing test was selected to detect the migration of C666-1 cells and Transwell test was used to detect the invasion of C666-1 cells.In addition,dual luciferase report experiment was used to detect the targeting relationship between circ_0072088 and miR-223.Results Compared with those in healthy subjects,the relative levels of circ_0072088 in the serum of patients with nasopharyngeal carcinoma were significantly increased(P＜0.05),however,the relative levels of miR-223 were significantly decreased(P＜0.05).Compared with those in control group and si NC group,the rate of proliferation inhibition,the apoptosis rate and the relative levels of miR223 of C666-1 cells in si circ_0072088 group were significantly increased(P＜0.05),while the colony formation number,the scratch distance and invasion number were significantly decreased(P＜0.05).Moreover,the dual luciferase report experiment confirmed that circ_0072088 was directly bound to miR-223.Conclusion Interfering circ_0072088 can inhibit the proliferation,migration and invasion of nasopharyngeal carcinoma cells,and its action mechanism may be related to the targeted upregulation of miR-223 expression.