Objective To study the anti-tumor effect of curcumin on breast cancer mice and its mechanism. Methods 4T1 mouse breast cancer cells were inoculated into mammary at pad of BALB/c mice for establishing the breast cancer mouse model. The tumor-bearing mice were divided into model group and curcumin low, medium and high dose (25, 50, 100 mg/kg) group. After 4 weeks of continuous administration, the tumor inhibition rate, spleen index and thymus index were calculated. The serum contents of interleukin-2 (IL-2), interleukin-12 (IL-12) and interleukin-α (TNF-α) were detected by enzyme-linked immunosorbent assay. The protein expression of phosphoinositide 3-kinase (PI3K), serine-threonine kinase (Akt), mammalian target of rapamycin (mTOR) and phosphorylation levels were detected by Western blotting. The effects of insulin-like growth factors-1 (IGF-1) which could activate PI3K, LY294002 which could inhibit PI3K and curcumin on the activity of mouse breast cancer cell 4T1 was detected by CCK-8 method, and to explore the effects of IGF-1, LY294002 and curcumin on PI3K/Akt/mTOR signaling pathway in 4T1 cells. Measurement data were expressed as Mean±SD, and t-test was used for comparison between groups. Results The tumor weight [(0.91±0.21), (0.83±0.18) vs. (1.18±0.24) g, t=2.820, P<0.05; t=3.846, P<0.01] of curcumin medium, high dose groups was lower than model group, and the tumor inhibition rate was 22.88% and 29.66%. The spleen index [(71.37±8.54), (75.79±8.87) vs. (63.21±5.74) mg/10 g, t=2.398, P<0.01; t=3.628, P<0.01 of curcumin medium, high dose groups and the thymus index [(28.46±4.74) vs. (23.33±2.78) mg/10g, t=3.254, P<0.01] of high dose group were higher than model group. The serum IL-2 contents [(139.55±16.95), (146.78±17.21) vs. (120.46±15.45) ng/L, t=2.819, P<0.05; t=3.859, P<0.01] and TNF-α contents [(53.46±6.89), (57.19±7.01) vs. (46.57±6.32) ng/L, t=2.493, P<0.05; t=3.811, P<0.01] of curcumin medium, high dose groups, and IL-12 contents [(163.24±18.73) vs. (148.26±16.31) ng/L, t=2.340, P<0.05] of high dose group were higher than model group. The p-Akt levels in tumor tissue [(0.69±0.12), (0.62±0.08) vs. (0.83±0.14), t=2.405, P<0.05; t=4.161, P<0.01] of curcumin medium, high dose groups, and p-PI3K levels [(0.62±0.11) vs. (0.75±0.13), t=2.537, P<0.05], p-mTOR levels [(0.56±0.11) vs. (0.69±0.17), t=2.098, P<0.05] were lower than the model group. The cell viability of 4T1 was 211.40%, 36.40% and 63.93% (t=11.890, P<0.01; t=16.160, P<0.01; t=8.742, P<0.01) after intervention with IGF-1, LY294002 and curcumin (100 μmol/L). The levels of p-PI3K, p-Akt and p-mTOR were increased in IGF-1 group (0.942±0.081, 0.894±0.093, 0.831±0.065, t=5.257, P<0.01; t=5.144, P<0.01; t=7.166, P<0.01) and IGF-1+ curcumin group (0.759±0.061, 0.751±0.058, 0.682±0.047, t=2.801, P<0.05; t=3.029, P<0.05; t=3.512, P<0.01) compared with the negative control group (0.671±0.082, 0.633±0.065, 0.583±0.042). Compared with the IGF-1 group, the levels of p-PI3K (t=3.153, P<0.05), p-Akt (t=2.917, P<0.05) and p-mTOR (t=4.154, P<0.01) in IGF-1+ curcumin group were decreased. Conclusion Curcumin can inhibit the breast cancer in mice and improve the immunity of the body, and its anti-tumor mechanism may be related to inhibition of PI3K/Akt/mTOR signaling pathway. Key words: Curcumin; Mouse breast cancer; Phosphoinositide 3-kinase/serine-threonine kinase/mammalian target of rapamycin signaling pathway