本研究的目的是调查circ_0000119在宫颈癌进展中的作用及其分子机制。采用定量实时聚合酶链反应（qRT-PCR）测量了宫颈癌组织和细胞系中circ_0000119、miR-433-3p和PAK2的表达水平。使用3-(4,5)-二甲基噻唑-5-基-橙（MTT）试验、5-乙炔基-2'-脱氧尿苷（EdU）试验和克隆形成试验评估细胞增殖。采用流式细胞术评估细胞周期和凋亡。通过Transwell试验检测细胞迁移和侵袭能力。使用在线生物信息学工具预测circ_0000119的下游结合靶点，并通过双荧光素酶报告基因测定、RNA免疫沉淀（RIP）试验和RNA pull-down试验进行确认。通过恢复实验探索circ_0000119/miR-433-3p/PAK2轴在调控宫颈癌过程中的作用。构建异种移植模型以进一步确定circ_0000119对宫颈癌肿瘤生长的影响。进行免疫组化（IHC）试验检测Ki67的表达。结果显示，在宫颈癌组织和细胞系中circ_0000119异常上调。 抑制circ_0000119能够抑制宫颈癌细胞的增殖，细胞周期进程，迁移和侵袭，并促进宫颈癌细胞凋亡。miR-433-3p是circ_0000119的结合靶点，PAK2是miR-433-3p的下游基因。miR-433-3p的抑制能够逆转沉默circ_0000119对宫颈癌进展的抑制作用。此外，PAK2的过表达逆转了miR-433-3p对宫颈癌进展的影响。PAK2的表达受circ_0000119和miR-433-3p调控。此外，circ_0000119的沉默减少了宫颈癌的肿瘤生长。circ_0000119在宫颈癌中上调，circ_0000119的沉默通过miR-433-3p/PAK2轴抑制了宫颈癌的恶性发展。© 2023. 作者(们)专属于波兰科学院植物遗传学研究所。

The purpose of this study was to investigate the role of circ_0000119 on CC progression and its molecular mechanism. The expression levels of circ_0000119, miR-433-3p, and p21-activated kinase 2 (PAK2) in CC tissues and cell lines were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay and colony formation assay. Cell cycle and apoptosis were assessed by flow cytometry. Cell migration and invasive ability were examined by Transwell assays. Downstream binding targets of circ_0000119 were predicted by online bioinformatics tools and confirmed by dual luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down assay. The role of circ_0000119/miR-433-3p/PAK2 axis in regulating the CC process was explored by rescue experiments. A xenograft model was constructed to further determine the effect of circ_0000119 on CC tumor growth in vivo. Immunohistochemistry (IHC) assay was conducted for Ki67 expression. Circ_0000119 was aberrantly upregulated in CC tissues and cell lines. Knockdown of circ_0000119 inhibited CC cell proliferation, cell cycle progress, migration, invasion, and promoted apoptosis of CC cells. MiR-433-3p was a binding target of circ_0000119, and PAK2 was a downstream gene of miR-433-3p. MiR-433-3p inhibition reversed the inhibitory effect of silencing circ_0000119 on CC progression. In addition, PAK2 overexpression reversed the effect of miR-433-3p on CC progression. PAK2 expression was regulated by circ_0000119 and miR-433-3p. Moreover, circ_0000119 knockdown reduced tumor growth of CC in vivo. Circ_0000119 was upregulated in CC, and circ_0000119 knockdown suppressed CC malignant development through the miR-433-3p/PAK2 axis.© 2023. The Author(s), under exclusive licence to Institute of Plant Genetics Polish Academy of Sciences.