Hospital of Stomatology, Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-Sen University, Guangzhou, Guangdong, China.
State Key Laboratory of Oncology in South China, MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China.
J Dent Res. 2020 Jun;99(6):666-675. doi: 10.1177/0022034520909312. Epub 2020 Apr 16.
Increasing evidence has revealed a significant association between microorganisms and oral squamous cell carcinoma (OSCC). , the keystone pathogen in chronic periodontitis, is considered an important potential etiologic agent of OSCC, but the underlying immune mechanisms through which mediates tumor progression of the oral cancer remain poorly understood. Our cohort study showed that the localization of in tumor tissues was related to poor survival of patients with OSCC. Moreover, infection increased oral lesion multiplicity and size and promoted tumor progression in a 4-nitroquinoline-1 oxide (4NQO)-induced carcinogenesis mouse model by invading the oral lesions. In addition, CD11b myeloid cells and myeloid-derived suppressor cells (MDSCs) showed increased infiltration of oral lesions. Furthermore, in vitro observations showed that MDSCs accumulated when human-derived dysplastic oral keratinocytes (DOKs) were exposed to , and CXCL2, CCL2, interleukin (IL)-6, and IL-8 may be potential candidate genes that facilitate the recruitment of MDSCs. Taken together, our findings suggest that promotes tumor progression by generating a cancer-promoting microenvironment, indicating a close relationship among , tumor progression of the oral cancer, and immune responses.
越来越多的证据表明，微生物与口腔鳞状细胞癌（OSCC）之间存在显著关联。牙龈卟啉单胞菌是慢性牙周炎的关键病原体，被认为是 OSCC 的一个重要潜在病因，但介导口腔癌肿瘤进展的潜在免疫机制仍知之甚少。我们的队列研究表明，肿瘤组织中 的定位与 OSCC 患者生存不良有关。此外，感染通过侵袭口腔病变，增加了 4-硝基喹啉-1 氧化物（4NQO）诱导的致癌发生小鼠模型中口腔病变的多发性和大小，并促进肿瘤进展。此外，CD11b 髓样细胞和髓源性抑制细胞（MDSCs）在口腔病变中的浸润增加。此外，体外观察表明，当人源性发育异常口腔角质形成细胞（DOKs）暴露于 时，MDSC 会积聚，趋化因子（CXCL2、CCL2）、白细胞介素（IL）-6 和 IL-8 可能是促进 MDSC 募集的潜在候选基因。总之，我们的研究结果表明， 通过产生促进癌症的微环境促进肿瘤进展，表明 、口腔癌的肿瘤进展和免疫反应之间存在密切关系。
