Huang Yu-Mei, Wang Lin-Qian, Liu Ying, Tang Fa-Qing, Zhang Wen-Ling
Department of Clinical Laboratory, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Clinical Laboratory of Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Hunan Key Laboratory of Oncotarget Gene, Changsha, Hunan, China.
Front Genet. 2022 Sep 14;13:935749. doi: 10.3389/fgene.2022.935749. eCollection 2022.
Immunotherapy is an individualized therapeutic strategy for nasopharyngeal carcinoma (NPC). However, few molecular targets are clinically satisfactory. This work aimed to integrate bulk and single-cell RNA sequencing data to identify novel biomarkers involved in NPC. We performed differentially expressed gene (DEG) analysis, Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and immune cell infiltration analysis prior to correlation analysis of the identified genes and immune cells and further assessed the prognostic effects of the biomarkers and immune cells in NPC. As a result, PKP1, a potential molecular biomarker associated with immune infiltration, and tumor-infiltrating lymphocyte-B cells (TIL-Bs) were identified as promising therapeutic targets for NPC. Importantly, immunohistochemistry (IHC) validated that PKP1 protein expression was mainly found in NPC cells rather than noncancerous cells. In addition, the tumor microenvironment (TME) of NPC was characterized by the infiltration of more dendritic cells (DCs) and γδT cells but fewer B cells. Our results suggest that the interaction of PKP1 and TIL-B cells is involved in NPC development. It is possible that TIL-B cells produce immunoglobulin G (IgG) to tumor antigens, such as PKP1, or viral antigens, including EBV and HPV, to execute antitumor ability through DC and T cells. In response, NPC cells express proteins such as PKP1 (absent in normal nasopharynx) to induce myeloid-derived suppressor cell (MDSC) expansion, which subsequently impairs the proliferation of B cells and results in B-cell death by generating iNOS and NOX2. In summary, our findings provide a potential therapeutic strategy for NPC by disrupting the interaction of PKP1 and TIL-Bs in the TME.
免疫疗法是鼻咽癌(NPC)的一种个体化治疗策略。然而,临床上令人满意的分子靶点很少。这项工作旨在整合批量和单细胞RNA测序数据,以鉴定参与鼻咽癌的新型生物标志物。在对鉴定出的基因和免疫细胞进行相关性分析之前,我们进行了差异表达基因(DEG)分析、基因本体(GO)富集分析、京都基因与基因组百科全书(KEGG)通路分析以及免疫细胞浸润分析,并进一步评估了这些生物标志物和免疫细胞在鼻咽癌中的预后作用。结果,鉴定出PKP1(一种与免疫浸润相关的潜在分子生物标志物)和肿瘤浸润淋巴细胞-B细胞(TIL-Bs)是鼻咽癌有前景的治疗靶点。重要的是,免疫组织化学(IHC)验证了PKP1蛋白表达主要存在于NPC细胞而非非癌细胞中。此外,鼻咽癌的肿瘤微环境(TME)的特征是树突状细胞(DCs)和γδT细胞浸润较多,而B细胞较少。我们的结果表明,PKP1与TIL-B细胞的相互作用参与了鼻咽癌的发展。TIL-B细胞可能产生针对肿瘤抗原(如PKP1)或病毒抗原(包括EBV和HPV)的免疫球蛋白G(IgG),通过DC和T细胞发挥抗肿瘤能力。作为回应,NPC细胞表达如PKP1(正常鼻咽中不存在)等蛋白质,以诱导髓源性抑制细胞(MDSC)扩增,随后损害B细胞的增殖并通过产生诱导型一氧化氮合酶(iNOS)和NADPH氧化酶2(NOX2)导致B细胞死亡。总之,我们的研究结果通过破坏TME中PKP1与TIL-Bs的相互作用,为鼻咽癌提供了一种潜在的治疗策略。