Abstract: Objective: To investigate the effect of lncRNA ZFPM2-AS1 targeting miR-519e-5p on the biological behavior of chordoma U-CH1 cells.Methods: U-CH1 cells were cultured in vitro; the small interfering RNA of ZFPM2-AS1 and the mimicry of miR-519e-5p were respectively transferred into U-CH1 cells, and then randomly divided into the following groups: si-NC group, si-ZFPM2-AS1 group, miR-NC group, miR-519e-5p group, si-ZFPM2-AS1+anti-miR-NC group, si-ZFPM2-AS1+anti-miR-519e-5p group; real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)was used to detect the expressions of lncRNA ZFPM2-AS1 and miR-519e-5p.MTT, flow cytometry, scratch assay, and Transwell assay were used to detect U-CH1 cell proliferation, apop-tosis, migration, and invasion, respectively.A dual-luciferase reporter assay was used to detect the targeted regula-tory relationship between lncRNA ZFPM2-AS1 and miR-519e-5p.Western blotting was used to detect the expres-sions of E-cadherin and N-cadherin.Results: Compared with the si-NC group and the miR-NC group, cell viabili-ty, scratch healing rate, the number of invasive cells and the protein level of N-cadherin in the si-ZFPM2-AS1 group and miR-519e-5p group decreased, while the apoptosis rate and E-cadherin level increased(P< 0.05).The lncRNA ZFPM2-AS1 could negatively regulate the expression of miR-519e-5p.Compared with si-ZFPM2-AS1+anti-miR-NC group, the cell viability, scratch healing rate, the number of invasive cells and the protein level of N-cadherin in si-ZFPM2-AS1+anti-miR-519e-5p group increased, while the apoptosis rate and E-cadherin level de-creased (P< 0.05).Conclusion: Down-regulation of lncRNA ZFPM2-AS1 can promote U-CH1 cell apoptosis and block proliferation, migration as well as invasion, the mechanism of which is related to up-regulation of miR-519e-5p expression.