Objective To investigate the mechanism of cell cycle regulation in intervening against the progression of cervical cancer based on the splicing factor 3B subunit 1（SF3B1）/forkhead box protein M1（FOXM1） axis. Methods SF3B1 overexpression in HeLa cells or SF3B1 knockdown in SiHa cells was achieved by transfection of SF3B1 overexpression plasmid（pSF3B1） and two SF3B1-specific short hairpin RNA（shSF3B1-1 and shSF3B1-2）. CCK-8 test and ethynyl-2′-deoxyuridine（EdU） were used to measure cell proliferation activity and proliferation rate；flow cytometry was used to observe cell cycle distribution；cell cycle PCR array，flow cytometry，chromatin co-immunoprecipitation-quantitative polymerase chain reaction（ChIP-qPCR），and luciferase experiments were used to clarify the targeting relationship between SF3B1 and FOXM1. Results After SF3B1 overexpression，there were significant increases in the growth rate and proliferation ability of HeLa cells（P<0.05）. In addition，there were significant reductions in the growth rate and proliferation ability of SiHa cells after SF3B1 knockdown（P<0.05）. In HeLa cells，compared with the pENTER group，the pSF3B1 group had a significant reduction in the G₀/G₁ ratio，while in SiHa cells，SF3B1 knockdown significantly increased the G₀/G₁ ratio. Furthermore，SF3B1 overexpression significantly promoted the expression of the G₁ phase-related protein cyclin D1 in HeLa cells，while SF3B1 knockdown significantly inhibited the expression of cyclin D1 in SiHa cells. Upregulation of SF3B1 significantly enhanced the expression of FOXM1，while downregulation of SF3B1 significantly inhibited FOXM1. ChIP-qPCR analysis showed the binding of SF3B1 to FOXM1 promoter site in HeLa cells. In the wild-type FOXM1 promoter，compared with the shNC group，the SF3B1 knockdown group had inhibition of luciferase activity（1.30±0.08 vs. 0.73±0.02 and 0.70±0.04，P<0.01），and the mutant FOXM1 promoter could not trigger a response to shSF3B1 in SiHa cells. The proliferation ability of HeLa cells was enhanced by SF3B1 overexpression（shNC+pENTER vs. shNC+pSF3B1：25.1±1.9 vs. 61.2±3.8，P<0.01） and was reduced by shFOXM1（shNC+pSF3B1 vs. shFOXM1+pSF3B1： 61.2±3.8 vs. 18.5±1.9，P<0.001），and the reduction in G0/G1 cycle induced by SF3B1 overexpression was partially reversed by FOXM1 knockdown（shNC+pSF3B1 vs. shFOXM1+pSF3B1：35.0±1.5 vs. 58.0±1.8，P<0.05）. Conclusion SF3B1 can be used as a tumor-promoting gene in cervical cancer，and it can promote the proliferation of cervical cancer cells and disrupt the cell cycle by upregulating the expression of FOXM1.