To observe the effects of Apigenin on the expressions of TGF-β1R II, NF-κB and VEGF genes in tumor tissues of mice with H29 colon cancer. Fifty ICR mice with H29 colon cancer were randomly divided into five groups: normal saline group, low-dose Apigenin group, middle-dose Apigenin group and high-dose Apigenin group and cyclophosphamide group. The mice were killed on the next day of administration discontinuance, and subcutaneous tumor tissues were collected. Quantitative fluorescence RT-PCR was used to detect the expression of TGF-β1R II, NF-κB and VEGF genes in tumor tissues of H29 colon cancer mice. Apigenin raised the expression level of TGF-β1R II in H29 colon cancer tissues, which showed the most obvious effect in the middle-dose group, with a significant difference compared with the normal saline group (P<0.01). The Apigenin group of each dose could significantly lower the NF-κB expression level in H29 colon solid tumors, showing significant differences compared with the normal saline group (P<0.01). The middle-dose and high-dose Apigenin groups could significantly reduce the level of VEGF expression in tumor tissues of ICR mice with H29 colon cancer, and the high-dose group had most obvious effect, and there were significant difference among the middle-dose group, high-dose group and the normal saline group (P<0.01). The mechanism of anti-tumor effect of Apigenin might be the reason that Apigenin can raise the expression level of TGF-β1R II by down-regulating the expression of NF–κB and VEGF in tumor tissues of tumor-bearing mice, thereby inhibiting tumor angiogenesis and tumor cell proliferation, so as to achieve the anti-tumor effect.