Authors
Zeyu Zhang, Jinxin Tao, Yifan Fu, Yi Dong, Yuanyang Wang, Menggang Zhang, Liyuan Ye, Jiangdong Qiu, Yueze Liu, Hao Chen, Jianchun Xiao, Hua Huang, Zhe Cao, Gang Yang, Taiping Zhang
Published in
Oncogenesis. Jun 27, 2026. Epub Jun 27, 2026.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains a highly aggressive malignancy driven by rapid metastasis and a profoundly immunosuppressive microenvironment. While the surface glycoprotein CD52 is a known immunoregulator, its precise role in solid tumors remains controversial, partly due to its broad expression across diverse cell populations and its compartment-specific functions within the tumor microenvironment. In this study, we utilized integrated single-cell RNA sequencing (scRNA-seq), functional assays, and compartment-specific clinical validation to elucidate the tumor-intrinsic functions of CD52 in PDAC. We identified a highly plastic, restricted subpopulation of CD52-high malignant epithelial cells that actively drives metastasis initiation by enhancing cellular invasive capacity. Concurrently, we demonstrated that tumor-derived CD52 orchestrated a multi-layered immunosuppressive network that attenuates CD8 + T cell cytotoxicity, facilitating early immune evasion. Furthermore, by systematically separating expression sources, our clinical validation established that tumor-derived CD52 is a prognostic indicator of poor patient survival. These findings characterize CD52 as a critical, tumor-intrinsic driver of PDAC progression, highlighting its value as a prognostic biomarker and a therapy target in combination with immune checkpoint blockade to overcome innate therapeutic resistance in PDAC.
PMID:
42364974
Bibliographic data and abstract were imported from PubMed on 28 Jun 2026.
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