Objective: To explore the role of MAPKs signal transduction system in the proliferation of human mammary carcinoma cell line MCF-7 induced by insulin. Methods:Human mammary carcinoma cell line MCF-7 was treated with different concentrations of insulin(0 nmol/L,25 nmol/L,50 nmol/L,100 nmol/L,200 nmol/L). MTT assay was used to explore the proliferation of MCF-7 cells with or without MAPKs signals blocked by their specific inhibitors which were SP600125, the inhibitor of the phosphorylation of JNK,and PD98059, the inhibitor of the phosphorylation of ERK1/2. The expressions of phospho-JNK and phospho-ERK1/2 at different time treated with insulin were detected by Western blot, and changes of those proteins expressions were observed when MAPKs signals blocker was added. Results:Insulin can promote the proliferation of MCF-7 cells in a concentration-dependent manner. Western blot result implicated that 100 nmol/L insulin induced the activation of JNK and ERK. The phosphrylation of JNK was detected beginning at 5 minutes after insulin treated and sustaining for an hour, while the activation of ERK was at the 30th minute after insulin treated and later than that of JNK. Then we reevaluated the proliferation effect promoted by insulin after MAPKs signaling pathway blocked by their inhibitors. The results showed that after the activities of JNK, ERK and JAK/STAT inhibited, the proliferation effect of insulin was also attenuated. Otherwise,Western blot result showed that, while blocking the MAPKs signaling pathway,10 μmol/L PD98059 could inhibit the activation of ERK1/2 induced by 200 nmol/L insulin,while 20 μmol/L SP600125 and 20 μmol/L AG490 couldn’t inhibit the activation of ERK1/2 obviously. Conclusion: Insulin can stimulate the proliferation of MCF-7 cells in vitro, and MAPKs signal transduction system involves in the proliferation of MCF-7 cells, which could mediate and promote mammary carcinoma development.