目的 探讨环状RNA circ-PHC3在宫颈癌组织中的表达及其对宫颈癌细胞增殖、迁移和侵袭行为的调控机制。 方法 通过GEO数据库分析circ-PHC3在宫颈癌组织和正常组织中表达，分析circ-PHC3表达与宫颈癌患者临床分期及预后的关系。实时定量聚合酶链反应（qRT-PCR）法检测circ-PHC3在宫颈癌细胞系HCC94、C33A、Hela、HCC1106、SiHa中的表达。选取表达最高的宫颈癌细胞转染circ-PHC3 inhibitor。双荧光素酶报告基因实验验证circ-PHC3和miR-1179之间的相互作用。qRT-PCR检测细胞中miR-1179表达。通过克隆形成实验、流式细胞术、划痕实验和Transwell实验检测细胞增殖、细胞周期、迁移和侵袭。Western blot法检测细胞中增殖、迁移和侵袭表型蛋白的表达。通过动物实验检测沉默circ-PHC3表达在体内对宫颈癌细胞生长和转移的作用。 结果 宫颈癌组织中circ-PHC3表达明显高于正常组织（P < 0.01），circ-PHC3表达与宫颈癌患者临床分期相关（P < 0.01），circ-PHC3高表达的宫颈癌患者生存率明显低于circ-PHC3低表达患者（P < 0.01）。宫颈癌细胞系HCC94、C33A、Hela、HCC1106、SiHa中circ-PHC3均表达升高（均P < 0.01），HCC1106细胞中circ-PHC3表达最高（P < 0.01）。circ-PHC3能够与miR-1179相互作用（P < 0.01），下调circ-PHC3能够促进miR-1179的表达（P < 0.01）。在HCC1106细胞中转染circ-PHC3 inhibitor后，细胞增殖、迁移和侵袭能力均显著降低（均P < 0.01），细胞周期被显著抑制（P < 0.01），该作用被miR-1179抑制剂部分逆转（均P < 0.05）。敲低circ-PHC3的HCC1106细胞中增殖、迁移和侵袭表型蛋白Cyclin E、CDK2、MMP-9、N-cadherin表达均降低（均P < 0.01），该作用被miR-1179抑制剂部分逆转（均P < 0.01）。敲低circ-PHC3能够在体内抑制HCC1106细胞的生长和转移（均P < 0.01）。 结论 circ-PHC3在宫颈癌组织中高表达，其表达升高与宫颈癌患者不良预后相关。敲低circ-PHC3能够上调miR-1179表达，抑制宫颈癌细胞的增殖、细胞周期、迁移和侵袭。

Objective To investigate the expression of the circular RNA circ-PHC3 in cervical cancer tissues and its regulatory mechanisms in the proliferation， migration， and invasion of cervical cancer cells. Methods The expression levels of circ-PHC3 in cervical cancer tissues and adjacent non-tumor tissues were analyzed using the GEO database. The correlation between circ-PHC3 expression and the clinical stage as well as prognosis of cervical cancer patients was also evaluated. The expression of circ-PHC3 in cervical cancer cell lines HCC94， C33A， HeLa， HCC1106， and SiHa was detected by real-time quantitative polymerase chain reaction （qRT-PCR）. The cell line with the highest circ-PHC3 expression was selected for transfection with a circ-PHC3 inhibitor. The interaction between circ-PHC3 and miR-1179 was validated using a dual luciferase reporter gene assay. The expression levels of miR-1179 in transfected cells were further assessed by qRT-PCR. Functional assays， including colony formation， flow cytometry， wound healing， and Transwell assays， were conducted to evaluate cell proliferation， cell cycle progression， migration， and invasion， respectively. Western blot analysis was performed to determine the expression of key proteins associated with proliferation， migration， and invasion in circ-PHC3-modulated cells. Finally， in vivo experiments were carried out to investigate the impact of circ-PHC3 silencing on the growth and metastasis of cervical cancer cells in animal models. Results The expression level of circ-PHC3 in cervical cancer tissues was significantly higher than that in adjacent normal tissues （P < 0.01）. Furthermore， circ-PHC3 expression was significantly associated with the clinical stage of cervical cancer （P < 0.01）. Patients with high circ-PHC3 expression exhibited a notably lower survival rate compared to those with low circ-PHC3 expression （P < 0.01）. In cervical cancer cell lines including HCC94， C33A， HeLa， HCC1106， and SiHa， circ-PHC3 expression was markedly upregulated （all P < 0.01）， with the highest expression observed in HCC1106 cells （P < 0.01）. Circ-PHC3 was found to directly interact with miR-1179 （P < 0.01）， and silencing circ-PHC3 significantly increased miR-1179 expression （P < 0.01）. Transfection of HCC1106 cells with a circ-PHC3 inhibitor significantly suppressed cell proliferation， migration， and invasion （all P < 0.01）， and induced cell cycle arrest （P < 0.01）； these effects were partially reversed by co-transfection with a miR-1179 inhibitor （all P < 0.05）. In HCC1106 cells with circ-PHC3 knockdown， the expression levels of key proteins associated with proliferation， migration， and invasion—Cyclin E， CDK2， MMP-9， and N-cadherin—were significantly reduced （all P < 0.01）， and this reduction was partially attenuated by miR-1179 inhibition （all P < 0.01）. In vivo experiments further demonstrated that circ-PHC3 knockdown significantly inhibited tumor growth and metastasis of HCC1106 cells （all P < 0.01）. Conclusions Circ-PHC3 is highly expressed in cervical cancer tissues， and its overexpression is significantly correlated with poor prognosis in patients with cervical cancer. Knockdown of circ-PHC3 upregulates the expression of miR-1179 and suppresses the proliferation， migration， and invasion of cervical cancer cells.