Establishment of human esophageal cancer xenograft model in immunocompetent mice and explorations of related immunological changes

[Background]To combine the primary cells of human esophageal cancer with a new type of three dimensional (3D) microcarrier 6, and then to inoculate the complex subcutaneously into immunocompetent mice. To establish a new animal xenograft tumor model of human esophageal cancer, and to explore the changes in the immune indicators of mice during tumor formation. [Methods] 1. Isolate and extract the primary cells of human esophageal squamous cell carcinoma (SCC); mix them well with the 3D microcarriers and fully incubate them. Then, inoculate the complex into the armpits of immunocompetent mice, and record the tumor formation rate and the pathological characteristics of xenograft tumors. 2. Isolate cells in the blood, bone marrow, and spleen of the experimental mice and the control mice, and detect changes in CD3+, CD4+, CD8+, myeloid-derived suppressor cells (MDSCs), and dendritic cells (DCs) by flow cytometry. [Results] The microcarrier 6-based model subcutaneously transplanted primary cells of human esophageal cancer, which further successfully grew into xenograft tumors in immunocompetent mice; the tumor formation rate was 80%. The hematoxylin-eosin (HE) staining and immunohistochemistry (IHC) characteristics indicated consistencies with the human esophageal cancer cells. The flow cytometry analysis showed that CD3+ and CD4+ cells in the peripheral blood and bone marrow of the tumor-formed mice were significantly reduced (P < 0.05). The cell counts of MDSCs and DCs in the blood, bone marrow, and spleen were elevated as compared with the control group, and with the MDSCs increased the most dramatically and statistically significant increase (P < 0.05). [Conclusion] The new type of 3D microcarriers were combined with human esophageal SCC cells; this model could be used to successfully construct an immunocompetent mouse xenograft model of human esophageal cancer. We further found that during tumor formation, the tumor cells may inhibit cellular immunity by regulating MDSCs, leading to tumor immunity escape and promoting tumor development.