Sun Yong, Wan Hong, Xiong Jie, Cao Kun, Yang Dashuai, Huang Jun
Department of Hepatobiliary and Pancreatic Surgery, Hefei First People's Hospital, Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Front Endocrinol (Lausanne). 2025 May 23;16:1559909. doi: 10.3389/fendo.2025.1559909. eCollection 2025.
The PCDH17 family has emerged as a prominent research focus in the field of oncology; however, the precise mechanism underlying the regulatory role of PCDH17 in shaping the inflammatory tumor microenvironment in pancreatic cancer remains elusive.
A thorough examination was carried out to explore the presence of PCDH17 in cancerous tumor tissues and its association with genes related to inflammation. Additionally, we comprehensively examined the association between PCDH17 and immune cell infiltration as well as immunotherapy in pancreatic cancer. Moreover, the single-cell data of pancreatic cancer was utilized for analyzing PCDH17 expression, cell differentiation, and intercellular communication.
PCDH17 exhibited differential expression across various tumor types. The low-expression group of PCDH17 showed reduced levels of inflammatory genes. Immunoinfiltration analysis indicated a significant association between T-cell infiltration and the expression of PCDH17. Analysis of single-cell sequencing data revealed that PCDH17 was primarily expressed in endothelial cells, with a decrease in expression observed during cellular differentiation trajectory. Notably, inflammation-related genes also displayed significant changes in their expression patterns along the endothelial cell differentiation trajectory. Cellular communication investigations unveiled multiple signaling pathways through which endothelial cells interacted with T cells. The presence of PCDH17 in endothelial cells was verified through various immunofluorescence techniques, and a simultaneous decline in its levels was observed alongside the decrease in inflammatory factors within the tumor microenvironment.
The predominant expression of PCDH17 was observed in endothelial cells, exhibiting a strong association with inflammatory genes and infiltration of immune cells. PCDH17 exhibits potential as a target for regulating the immune-suppressive tumor microenvironment in pancreatic cancer.
PCDH17家族已成为肿瘤学领域的一个重要研究焦点；然而，PCDH17在塑造胰腺癌炎性肿瘤微环境中发挥调节作用的精确机制仍不清楚。
进行了全面的检查，以探究PCDH17在癌组织中的存在情况及其与炎症相关基因的关联。此外，我们全面研究了PCDH17与胰腺癌中免疫细胞浸润以及免疫治疗之间的关联。此外，利用胰腺癌的单细胞数据来分析PCDH17的表达、细胞分化和细胞间通讯。
PCDH17在不同肿瘤类型中表现出差异表达。PCDH17低表达组的炎症基因水平降低。免疫浸润分析表明T细胞浸润与PCDH17的表达之间存在显著关联。单细胞测序数据分析显示，PCDH17主要在内皮细胞中表达，在细胞分化轨迹中表达下降。值得注意的是，炎症相关基因在沿着内皮细胞分化轨迹的表达模式中也显示出显著变化。细胞通讯研究揭示了内皮细胞与T细胞相互作用的多种信号通路。通过各种免疫荧光技术验证了PCDH17在内皮细胞中的存在，并且观察到其水平随着肿瘤微环境中炎症因子的减少而同时下降。
观察到PCDH17主要在内皮细胞中表达，与炎症基因和免疫细胞浸润密切相关。PCDH17具有作为调节胰腺癌免疫抑制性肿瘤微环境靶点的潜力。
