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To study the anti-tumor effect and possible mechanism of Dichloromethane extraction of Caesalpinia minax Hance (DECH) on HepG2 cells and H22 tumor-bearing mice. MTT assay, hoechst33258 staining and scratch test were used to analyze the inhibitory effect of DECH on HepG2 cells in vitro. Fifty male kunming mice were subcutaneously inoculated with H22 cells to establish tumor-bearing mouse model. Another 10 mice were taken as the normal group. The corresponding drugs were given for 14 days respectively. The body weight and tumor weight were measured. The tumor inhibition rate, thymus and spleen index were calculated. Serum alpha fetoprotein (AFP) and IL-6 levels and liver and kidney function were detected. The expression of STAT3,Bax and bcl-2 protein in tumor tissues were detected by western blot. In vitro results showed that IC50 values at 12 h, 24 h, and 48 h were 43. 34±3. 46 μg/mL,32. 61±1. 60 μg/mL,and 27. 68±1. 23 μg/mL,respectively. DECH can inhibit the migration of HepG2 cells. The results of in vivo experiments show that, compared with the model group, the tumor quality of mice in each dose group of DECH was significantly reduced (P<0. 01,P<0. 05),and the tumor inhibition rates of low, medium and high dose groups were 27. 87%,39. 71% and 53. 22%,respectively. The thymus index in the DECH high-dose group was significantly increased, and the spleen index was significantly decreased (P<0. 01,P<0. 05) . The serum AFP and IL-6 content in the high dose group were also significantly reduced (P<0. 01,P<0. 05) . At the same time, the liver and kidney function of mice in the DECH administration group was improved, the expression of STAT3 and Bcl-2 protein was significantly reduced (P<0. 01),and the expression of Bax was significantly increased (P<0. 01) . The above results showed that DECH may inhibit the growth of HepG2 cells in vitro by inhibiting cell proliferation and affecting cell migration. Inhibition of tumor growth in H22 Tumor bearing mice in vivo may be related to inhibition of IL-6/STAT3 signaling pathway and promotion of tumor cell apoptosis. [ABSTRACT FROM AUTHOR]