Abstract： Objective To investigate the anti-apoptosis effects of EG-VEGF on pancreatic cancer cell MiaPaCa and its molecular mechanism. Methods The cells were treated with 50, 100, 200 ng/ml EG-VEGF. Flow cytometry was used to determine the apoptosis. The expression of p42/44MAPK, STAT3 protein and the phosphorylation, and anti-apoptosis protein Mcl-1 was evaluated by Western blot. Non-specific G protein-coupled receptor antagonist PTX, Rsa/ERK signal transduction blockade PD98059, JAK/STAT3 signal transduction blockade AG490 were used to treat the cells for 1 h, and the change of Mcl-1 protein was observed. Results After treated with 50 ng/ml EG-VEGF, the apoptosis rate of MiaPaCa was decreased from (28.4 ±4.6)% to (13.21 ±4.65)% (P<0.05) ; the phosphorylation of p42/44MAPK increased by 1.735 ± 0.019 folds; the phosphorylation of STAT3 increased by 21.810 ± 0.052 folds; the expression of Mcl-1 protein increased by 3.460 ±0.002 folds when compared with that of control group,and the difference was statistically significant (P < 0.05 ). But the degree of phosphorylation and the expression of Mcl-1 were not further increased with 100, 200 ng/ml EG VEGF treatment. After PTX pre-treatment, the increase of Mcl-1 protein expression was completely inhibited, and after PD98059, AG490 pre-treatment, the increase of Mcl-1 expression was inhibited to 52% and 68%. Conclusions EG-VEGF can inhibit MiaPaCa cell from apoptosis,and the mechanism may be related with activation of Ras MAPK and JAK STAT3 signal transduction pathway and up-regulation of Mcl-1.