Fig. 4

The melittin-MIL-2 inhibited tumor growth and exhibited enhanced antitumor activity compared to rIL-2 in vivo. These cancer cells (SMMC-7721: 5 × 10⁶ cells per animal, A549: 5 × 10⁶ cells per animal, SKOV3: 2 × 10⁵ cells per animal) were subcutaneously injected into female BALB/c mice (6 week-old). When tumors became palpable (5–7 days), the mice (n = 5 per group) were randomized into groups and administered intraperitoneally at the indicated time points with the melittin-MIL-2 (200 μmol per animal) or rIL-2 (200 μmol per animal) or melittin (200 μmol per animal). Tumor volumes were measured twice a week. As soon as mice produced ascites and had a weight increase >30 %, they were killed. The xenograft model (liver SMMC-7721 cancer) was used to observe the mice survival. We carefully observed and recorded the survival of each mouse, and calculated overall survival. a After day 16, mean tumor volumes among treatment groups were statistically different (p < 0.05). Melittin-MIL-2 therapy was conspicuously different than control (saline) from day 16 to the end of the experiment (p < 0.05). Moreover, melittin-MIL-2 treatment was significantly different than rIL-2 treatment from day 20 to the conclusion of the experiment (p < 0.05). b, c After day 12, mean tumor volumes among treatment groups were statistically different (p < 0.05). Melittin-MIL-2 therapy was significantly different than control from day 12 to the conclusion of the experiment (p < 0.05). Furthermore, melittin-MIL-2 therapy was evidently different than rIL-2 therapy from day 23 to the end of the experiment (p < 0.05). d The survival time among the mice treated with melittin-MIL-2 was higher than other groups (p < 0.05)