As metformin can inhibit endometrial carcinoma (EC) cell growth and the insulin growth factor (IGF)system is active in EC, the question of whether t can regulate endometrial carcinoma cell secretion of IGF-1or expression of IGF-1 receptor (IGF-1R) is of interest. In this study, serum IGF-1 levels in EC patients werefound to be comparable with that in the non EC patients (p>0.05). However, the IGF-1 level in the medium ofcultured cells after treatment with metformin was decreased (p<0.05). IGF-1R was highly expressed in humanendometrial carcinoma paraffin sections, but IGF-1R and phosphor-protein kinase B/protein kinase B (p-Akt/Akt) expression was down-regulated after metformin treatment (p<0.05). In summary, metformin can reduce thesecretion of IGF-1 by Ishikawa and JEC EC cell lines and their expression of IGF-1R to deactivate downstreamsignaling involving the PI-3K/Akt pathway to inhibit endometrial carcinoma cell growth.