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目的:探讨miR-193b通过靶向调节cyclin D1对宫颈癌细胞放疗敏感性的影响。方法:河北北方学院附属第一医院2019年5月至2020年5月收治的20例宫颈癌患者被纳入研究，取其宫颈癌组织和癌旁组织，qRT-PCR检测miR-193b与cyclin D1在宫颈癌组织的表达。筛选耐辐射HeLa细胞，另外干预HeLa细胞中miR-193b和cyclin D1的表达并将细胞分为如下组：空白对照组、miR-NC组、miR-193b mimics组、miR-193b过表达+PCDNA-cyclin D1 NC组、miR-193b过表达+PCDNA-cyclin D1组。观察miR-193b对耐辐射HeLa细胞增殖能力及细胞周期的影响。双荧光素酶实验验证miR-193b与cyclin D1的靶向关系。挽救实验检测miR-193b是否通过抑制cyclin D1调控细胞周期。结果:与癌旁组织相比，宫颈癌组织中的miR-193b水平明显降低（n P=0.007），cyclin D1水平显著升高（n P=0.003）；与对照组[（1.89±0.13）（2.73±0.18）（3.37±0.26）]相比，耐辐射HeLa细胞转染miR-193b mimics后，细胞48、72、96 h的增殖能力[（0.72±0.04）（1.63±0.14）（2.05±0.17）]明显降低（n P<0.05）。相对于miR-NC组（51.53%±3.71%），过表达miR-193b能够导致细胞G1期（62.95%±4.15%）阻滞（n P<0.05）。cyclin D1是miR-193b的靶基因。挽救实验证实miR-193b通过cyclin D1调控细胞周期。n 结论:过表达miR-193b水平能降低耐辐射HeLa细胞增殖能力，提高放疗的敏感性，其作用机制可能是通过下调Cyclin D1表达，诱导细胞周期G1期阻滞。“,”Objective:To investigate the effects of miR-193b on radiosensitivity of cervical cancer cells by targeting Cyclin D1.Methods:20 patients with cervical cancer treated in the First Affiliated Hospital of Hebei Northern University were enrolled in this study, and their cancer tissues and paracancerous tissue were collected. The expressions of miR-193b and Cyclin D1 in cervical cancer tissue were detected by qRT-PCR. Radiation-resistant HeLa cells were screened, and the expression of miR-193b and cyclin D1 in HeLa cells were intervened and then divided the cells into the following groups: Blank group, miR-NC group、miR-193b mimics group、miR-193b mimics+PCDNA-cyclin D1 NC group、miR-193bmimics+PCDNA-cyclin D1 group. The effects of miR-193b on radiosensitivity, cell proliferation and cell cycle were observed. Double luciferase assay was used to verify the targeting relationship between miR-193b and Cyclin D1. Rescue test was used to detect whether miR-193b regulated cell cycle by inhibiting Cyclin D1.Results:Compared with paracancerous tissues, the level of miR-193b in cervical cancer tissue was significantly decreased (n P=0.007) , while the level of cyclin D1 was significantly increased (n P=0.003) . Compared with control group[ (1.89±0.13) (2.73±0.18) (3.37±0.26) ], the cell proliferation ability was significantly decreased when radiation-resistant HeLa cells were transfected with miR-193b mimics (0.72±0.04) (1.63±0.14) (2.05±0.17) at 48, 72, and 96 h (n P<0.05) .Compared with miR-NC group, overexpression of miR-193b can lead to cell cycle arrest at G1 phase (62.95%±4.15%) (n P<0.05) . Cyclin D1 was the target gene of miR-193b. Rescue experiments confirmed that miR-193b regulated cell cycle through cyclin D1.n Conclusions:Overexpression of miR-193b can reduce the proliferation of radiation-resistant HeLa cells and improve the sensitivity of radiotherapy. The mechanism may be through down regulating Cyclin D1 expression to induce cell arrest G1 phase.