#0907

SPRR1B+ Epithelial-like endothelial cells promoting the malignant progression of Penile squamous cell carcinoma

T. Tao1, D. Shen2

1The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Department of Urology, Hefei, China
2The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Department of Urolog, Hefei, China

Introduction:

The heterogeneity, developmental differentiation trajectories, and underlying molecular mechanisms of endothelial cells in penile squamous cell carcinoma (PSCC) remain inadequately understood. This study aims to further explore the heterogeneity of endothelial cells in penile cancer at single-cell resolution and investigate their potential contribution to tumor progression.

Material and methods:

We collected matched tumor and adjacent normal tissue samples from five PSCC patients and performed single-cell RNA sequencing. Next, we employed multiplex immunofluorescence (mIF) staining to confirm the presence of SPRR1B+ endothelial cells (ECs) in tumor tissue from 34 penile cancer patients. We then explored the potential effects of PSCC tumor cells on endothelial cells through co-culture experiments and further investigated the biological role of SPRR1B+ ECs in the progression of PSCC in vitro.

Results:

In this study, we utilized single-cell RNA sequencing to profile the cellular landscape of PSCC. We identified a new subpopulation of endothelial cells (SPRR1B+ ECs) that highly expresses the epithelial cell marker SPRR1B. SPRR1B+ ECs are significantly upregulated in PSCC tumor tissues, particularly in the later stages of tumor progression. Clinical cases showed that high expression of SPRR1B+ ECs is associated with poor prognosis. Furthermore, functional experiments demonstrated that SPRR1B+ ECs promote the malignant progression of PSCC tumor cells through direct cell-cell contact.


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    上傳者
    TUA線上教育_家琳
    單位
    台灣泌尿科醫學會
    建立
    2026-04-24 17:03:04
    最近修訂
    2026-04-24 17:03:12
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