期刊
PATHOLOGY & ONCOLOGY RESEARCH
卷 28, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/pore.2022.1610555
关键词
cancer; metastasis; natural killer cell; Nocardia rubra cell-wall skeleton; cytotoxicity
资金
- Scientific Research Fund of Liaoning Provincial Education Department
- [JYTJCZR2020053]
The study found that the biological macromolecule Nocardia rubra cell-wall skeleton (Nr-CWS) can suppress lung metastasis induced by B16F10 melanoma cells, possibly by promoting NK cell terminal differentiation and upregulating the production of cytokines and cytotoxic molecules.
The biological macromolecule Nocardia rubra cell-wall skeleton (Nr-CWS) has well-established immune-stimulating and anti-tumor activities. However, the role of Nr-CWS on natural killer (NK) cells remains unclear. Here, we explore the function and related mechanisms of Nr-CWS on NK cells. Using a tumor-bearing model, we show that Nr-CWS has slightly effect on solid tumor. In addition, using a tumor metastasis model, we show that Nr-CWS suppresses the lung metastasis induced by B16F10 melanoma cells in mice, which indicates that Nr-CWS may up-regulate the function of NK cells. Further investigation demonstrated that Nr-CWS can increase the expression of TRAIL and FasL on spleen NK cells from Nr-CWS treated B16F10 tumor metastasis mice. The spleen index and serum levels of TNF-alpha, IFN-gamma, and IL-2 in B16F10 tumor metastasis mice treated with Nr-CWS were significantly increased. In vitro, the studies using purified or sorted NK cells revealed that Nr-CWS increases the expression of CD69, TRAIL, and FasL, decreases the expression of CD27, and enhances NK cell cytotoxicity. The intracellular expression of IFN-gamma, TNF-alpha, perforin (prf), granzyme-B (GrzB), and secreted TNF-alpha, IFN-gamma, IL-6 of the cultured NK cells were significantly increased after treatment with Nr-CWS. Overall, the findings indicate that Nr-CWS could suppress the lung metastasis induced by B16F10 melanoma cells, which may be exerted through its effect on NK cells by promoting NK cell terminal differentiation (CD27(low)CD11b(high)), and up-regulating the production of cytokines and cytotoxic molecules.
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