AIM: To explore the effect and mechanism of circZNF124 on the proliferation, migration and invasion of colorectal cancer SW620 cells. METHODS: The expression levels of circZNF124 and miR-4262 in colorectal cancer tissues were measured by qRT-PCR method. Human colorectal cancer cells SW620 were cultured in vitro, and were randomly grouped into si-NC group, si-circZNF124 group, miR-NC group, miR-4262 group, si-circZNF124 j anti-miR-NC group, si-circZNF124 j antimiR-4262 groups. CCK-8 method, plate clone formation test, scratch test and Transwell test respectively were used to detect cell proliferation, clone formation, migration and invasion of SW620 cells. The dual luciferase reporter experiment analyzed the targeted binding of circZNF124 to miR-4262. Western blot was used to detect the expression of E-cadherin and N-cadherin protein. RESULTS: The expression of circZNF124 in colorectal cancer tissue was increased by about 3.75 times compared with that in the adjacent tissue (P i 0.05), and the expression of miR-4262 was decreased by about 0.73 times compared with the adjacent tissue (P i 0.05). Compared with the si-NC group, the cell viability, scratch healing rate and the protein level of N-cadherin in the si-circZNF124 group were decreased (P i 0.05), the number of cell clone formation and the number of invasive cells were decreased (P i 0.05), while the protein level of E-cadherin was increased (P i 0.05). circZNF124 could negatively regulate the expression of miR-4262. Compared with the miR-NC group, the cell viability, scratch healing rate and the protein level of N-cadherin in the miR-4262 group were reduced (P i 0.05), the number of cell clones and the number of invasive cells were reduced (P i 0.05), while the protein level of E-cadherin was increased (P i 0.05). Inhibition of miR-4262 expression reversed the effect of interfering circZNF124 expression on the proliferation, migration and invasion of SW620 cells.CONCLUSION: Interference with the expression of circZNF124 can attenuate the proliferation, migration and invasion of colorectal cancer cells by targeting miR-4262.