Promotes Immunoevasion of Oral Cancer by Protecting Cancer from Macrophage Attack.

The relationship of and oral squamous cell carcinoma (OSCC) has been studied for several years. Previous studies have focused on the direct effect of on the activities of primary epithelial cells and OSCC cells. However, the immune system is responsible for mediating cancer development, whether can affect oral cancer immunity has seldom been explored to date. In this study, we investigated the role of in the immunoevasion of OSCC. We evaluated the effect of on the phagocytosis of Cal-27 cells (OSCC cell line) by bone marrow-derived macrophages in vitro and studied the effect of on the growth of OSCC and the polarization of tumor-associated macrophages in vivo. We found that was able to inhibit the phagocytosis of Cal-27 cells by macrophages, and membrane-component molecules of , such as proteins, were speculated to be the effector components. In addition, sustained infection with antibiotics-inactivated promoted OSCC growth in mice and induced the polarization of macrophages into M2 tumor-associated macrophages, which mainly display protumor properties. Transcriptome analysis and quantitative RT-PCR revealed that infection upregulated the expression of genes encoding protumor molecules in Cal-27 cells (, , and ) and in macrophages (, , and ). Our in vitro and in vivo data suggest that can promote immunoevasion of oral cancer by protecting cancer from macrophage attack. To our knowledge, the present study reveals a novel mechanism by which promotes OSCC development.