Objective:To observe the effect of insulin on PI3K and Erk signaling pathway and its regulation of proliferation and migration in K562 cells. Methods: K562 cells were treated with insulin with different concentrations (0, 25, 50, 100 and 200 nmol/L) for 48 h, and 200 nmol/L insulin for 0, 12, 24 and 48 h. Then, the phosphorylation levels of PI3K and Erk were detected by Western blot, and the proliferation ability of K562 cells was detected by MTT. Effect of insulin on migration ability of K562 cells was detected by wound healing assay. K562 cells were pretreated with PI3K and Erk signaling pathway inhibitors LY294002 and U0126 to observe the effect of PI3K and Erk signaling pathway on insulin induced proliferation and migration in K562 cells. Results: Compared with the 0 nmol/L insulin treated group, 25, 50, 100 and 200 nmol/L insulin treated groups had significantly increased phosphorylation levels of PI3K and Erk and promoted proliferation in K562 cells (P < 0.01). Compared with the 0 h insulin treated group, 200 nmol/L insulin treated for 12, 24 and 48 h groups also had significantly increased phosphorylation levels of PI3K and Erk and promoted proliferation in K562 cells (P < 0.01). After treated with 200 nmol/L insulin by 48 h, the migration ability of K562 cells were significantly increased (P < 0.01). After blocked PI3K and Erk signaling pathway by LY294002 and U0126, the ability of insulin in induced proliferation and migration in K562 cells were significantly decreased (P < 0.01). Conclusion: Through actives PI3K and Erk signaling pathway, insulin can promote proliferation and migration of K562 cells.