TGIF ( TG interacting factor) is an inhibitor of TGF-βsignaling pathway. However, TGF-β can overcome the cell growth in the early stage of tumorigenesis, but promote the invasion and metastasis of neoplasms in the later stage. However its role in carcinogenesis is still unknown. After gastric carcinoma cell line, SGC-7901, was stablely transfected with plasmid PcDNA3.1-TGIF, the effect of TGIF on it was investigated via MTT method, flow cytometry, plate clone formation, nude mice tumorigeneity and the expressions of MMP2, MMP9 and VEGF proteins were detected in tumors originated from inoculated TGIF transfected, PcDNA3.1 transfected and SGC-7901 cells via immunohistochemistry. The contents of VEGF, active MMP2 and MMP9 in supernants of three cells were examined via ELISA and zymograph respectively. TGIF has no effect on the proliferation, cell cycle distribution and plating efficacy of SGC-7901 cells. In vivo experiment, tumors originated from TGIF transfected cells have no embolism formed inside whereas tumors originated from control cells have obvious embolisms. The expression levels of MMP9 and VEGF in tumors from TGIF transfectant cells are less than that from appropriate control cells, whereas MMP2 has no detectable difference among the three cells. The concentrations of VEGF in supernants of TGIF transfectant, PcDNA3.1 transfectant and SGC-7901 cells were (635±20.3) ng/L, (780±25.4) ng/L and (791±23.9) ng/L respectively. The content of VEGF in TGIF transfectant cells was significantly lower than that in control cells (P < 0.01). The contents of active MMP9 protein in supernants of TGIF transfectant cells were also significantly lower than that in control cells. Although TGIF can partially resist TGF-β mediated growth inhibition, it can not worsen the biological behaviors of gastric cancer cells. Inversely, TGIF can downregulate the expressions of VEGF and MMP9 and then mitigate their metastasis.