Fig. 5

iRGD-modified P-CIML NK cells effectively controlled tumor growth. A Experimental scheme of the antitumor experiment in vivo. Five-week-old female Babl/c-nude mice were subcutaneously injected with 5 × 10⁶ HepG2 cells to initiate an antitumor experiment in vivo. After two weeks, 2 × 10⁷ P-CIML NK (PBMCs were primed with IL-12, IL-15, and IL-18) cells or P–c-NK (PBMCs primed with low concentration IL-15) modified with iRGD or not were injected into the mice. This was followed by IL-2 treatment every other day for approximately 10 times, with 4 or 5 mice in each treatment group. The tumor burden of the mice was monitored. B Histograms showing the expression of αvβ3, αvβ5 and NRP-1 on HepG2 cells. C Imaging of mice with subcutaneous HepG2 tumors was conducted in vivo at various intervals post intravenous injection of CIML NK (sorted CD56 + cells) cells, which had been modified with or without iRGD. Magenta dashed lines indicate tumors. CIML NK cells labeled with DiR. D The percentage of human CD56 + cells in the tumor tissue of CIML NK-iRGD or control CIML NK-treated mice detected by flow cytometry at 24h after intravenous injection of NK cells. E Summary of data from D showing CD56 + NK cells among total cells. F The tumor volume of the mice treated with P–c-NK or P-CIML NK modified with or without iRGD. G Photos of tumors harvested from mice in all groups on day 28 after tumor inoculation. The average tumor volume (H) and tumor tissue weight (I) in different groups at the endpoint of the animal experiment. J The average weight of different groups for 28 days. Statistical significance was calculated by one-way analysis of variance (ANOVA) represented as mean ± s.e.m. NRP-1 Neuropilin-1, s.c. subcutaneous injection, i.v. intravenous injection, i.p. intraperitoneal