State Key Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
Department of Cariology and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
J Immunol. 2020 Jul 1;205(1):282-289. doi: 10.4049/jimmunol.1901138. Epub 2020 May 29.
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.
和口腔鳞状细胞癌（OSCC）的关系已经研究了好几年。以前的研究集中在直接影响原发性上皮细胞和 OSCC 细胞的活性。然而，免疫系统负责介导癌症的发展，到目前为止，还很少有研究探讨是否可以影响口腔癌的免疫。在这项研究中，我们研究了在 OSCC 的免疫逃避中的作用。我们评估了对骨髓来源的巨噬细胞体外吞噬 Cal-27 细胞（OSCC 细胞系）的影响，并研究了对 OSCC 生长和肿瘤相关巨噬细胞极化的体内影响。我们发现能够抑制巨噬细胞对 Cal-27 细胞的吞噬作用，并且推测膜成分分子，如蛋白质，是效应成分。此外，持续感染抗生素失活的促进了小鼠中 OSCC 的生长，并诱导巨噬细胞向 M2 肿瘤相关巨噬细胞极化，后者主要表现出促肿瘤特性。转录组分析和定量 RT-PCR 显示，感染上调了 Cal-27 细胞（、和）和巨噬细胞（、和）中编码促肿瘤分子的基因表达。我们的体外和体内数据表明，通过保护癌症免受巨噬细胞攻击，可促进口腔癌的免疫逃避。据我们所知，本研究揭示了促进 OSCC 发展的新机制。
