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To explore the biological role and mechanism of DACH1 in liver cancer, and to provide help for the early diagnosis, treatment and prognosis evaluation of liver cancer. Methods Immunohistochemical method was used to detect the expression level of DACH1 in 30 cases of liver cancer tissues and matched normal tissue samples. The Western Blot method was used to detect DACH1 and screen for low expression DACH1 in hepatocellular carcinoma cell lines. The HepG2 cell line overexpressing DACH1 was constructed by lentivirus and the expression effect of DACH1 was verified by Western Blot method. CCK8 was used to detect the proliferation of HepG2 cell lines with high expression of DACH1 at 24, 48, 72 and 96 hours. Flow cytometry was used to detect the cycle change of HepG2 cell line with high expression of DACH1. Western Blot method was used to detect the expression of CyclinD1, CDK4, CyclinE1, and CDK2. The HepG2 cell line with high expression of DACH1 was used to observe the proliferation in vivo using nude mouse xenograft tumor model and to verify DACH1 in tumor by immunohistochemistry. Results DACH1 was lower than normal tissues in liver cancer tissues (P < 0.001); DACH1 expression was lower than normal liver cell lines in liver cancer cells, and HepG2 shawed the lowest expression in HepG2, Hep3B, Huh7 cell lines (P < 0.05). The proliferation of HepG2 cell line with high expression of DACH1 was significantly lower than that of control cells (P < 0.05), indicating that the growth of cells with high expression of DACH1 was obviously inhibited. DACH1 up-regulated cells showed more cells in G0 / G1 phase, while fewer cells in S phase compared with control cells (P < 0.01), and there was no significant difference between the two in G2 / M phase. DACH1 up-regulated cells showed down-regulated expression of cycle-related proteins CyclinD1, CDK4, CyclinE1, and CDK2 (P < 0.05). Demonstrating that DACH1 blocks cell cycle progression by affecting cycle-related proteins. The HepG2 cell line highly expressing DACH1 resulted in approximately three-fold reduction in tumor weight compared with control cells. Measurement of tumor volume at 0, 3, 6, and 9 days after tumor formation showed that the growth rate of HepG2 cell line with high expression of DACH1 was significantly slowed (P < 0.05). Conclusion DACH1 can inhibit the proliferation of hepatoma cell line HepG2 and tumorigenesis in nude mice; DACH1 inhibits hepatoma cells by suppressing cyclin to induce cell cycle G1 / S block. DACH1 inhibition of hepatoma cells mainly blocks G1/S cell progression by inhibiting cycle-related proteins [ABSTRACT FROM AUTHOR]