Tumor patients are characterized with an abnormal immune function, with majority of the patients having low immunity. Some have enforced incomplete tumor resection where the surgery wound also heals normally. This is a common clinical phenomenon. In tumor cells that can secrete a strong cytokines pattern, the residual tumor cells particularly release
a large amount of cytokines BIBW2992 datasheet after incomplete resection, which stimulate the surrounding tissue under repair, thus speeding up the wound healing process. This involves the vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and other cytokines [3, 6]. This makes the question on whether the influence of surgery wounds on tumor cells depresses or promotes proliferation in tumor cells, interesting. To evaluate the relationship between acute inflammation or wound healing and tumor growth, this study utilizes a mouse tumor model with a manufactured surgical wound. The model is BMS202 manufacturer capable of building a representation of acute inflammation. Present in this Rabusertib mouse model are the inhibitory effects on tumor growth of acute inflammation in the early stage, which is the functional
reaction of IFN-γ due to wound inflammation. In the latter stage, the role of the tumor is to resist IFN-γ by releasing TGF-β to balance the inflammatory factor effect on the tumor cells. Similar to real situations, a pair of cytokines IFN-γ/TGF-β established a new balance to protect the tumor from the interference factor of inflammation. Likewise, a new Lck immune escape mechanism in the tumor cells occurred because of increased access to cell proliferation. Our in vitro and
in vivo experiments confirmed a new view of clinical surgery that will provide more detailed information to evaluate tumors after surgery. The study also offers a better understanding of the relationship between tumor and inflammation, as well as tumor cells and attacks on immunity. Materials and methods Cells and Animals Cells: Mouse melanoma cell-line B16F10 was supplied by the Department of Cell Biology, Huanhu Hospital, Tianjin, People’s Republic of China. The cell was cultured in RPMI1640 medium (Hyclone) containing 10% fetal bovine serum (FBS: Gibco), 50 units/ml penicillin, and 50 μg/ml streptomycin (Gibco). In all the experiments, the cell was maintained in 100 mm culture dishes (Costar) at 37°C in humidified 5% CO2/95% air atmosphere. Animals: female six-week old, 18~22 g C57/BL mice were purchased from the Animal Center Academy of Military Medical Science (License: SCXK [Jin] 2004-0001; Beijing, China). They were brought to the Animal Centre of Tianjin Medical University one week before the experiment and were bred under the specific pathogen-free (SPF) conditions.