ORIGINAL RESEARCH article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1655980
This article is part of the Research TopicExploring immune low-response states through single-cell technologies and spatial transcriptomicsView all 19 articles
Thymidine Kinase 1 Related to Prolif-like T cells Promoted GBM through Regulation of Cell ycle and EMT Signals: A Comprehensive Research based on Multi-omics Analysis and Experimental Validation
Provisionally accepted
- 1First Affiliated Hospital, Dalian Medical University, Dalian, China
- 2Panjin Central Hospital, Panjin, China
- 3The Second Hospital of Dalian Medical University, Dalian, China
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Background: Glioblastoma (GBM) is a common high-grade glioma characterized by a significantly immuno-suppressed immune microenvironment. Prolif-like T cells are a subset of T cells whose expression of related markers can influence the tumor microenvironment. Methods: This study used scRNA-seq and stRNA-seq to identify markers associated with Prolif-like T cells in the GBM tumor microenvironment. Survival analysis and consistency clustering were then employed to identify GBM subtypes associated with Prolif-like T cells, followed by an analysis of differences between subtypes. This study constructed survival models and scRNA-seq to screen for important genes associated with Prolif-like T cells in GBM and further investigated the role of TK1 in the cell cycle and EMT processes of GBM. Results: Using scRNA-seq from 149002 GBM cells, our study identified 593 Prolif-like T cell-related markers. The results of stRNA-seq revealed the close association of Prolif-like T cell with cell cycle and EMT signals. In addition, 82 genes were found to influence GBM prognosis. Based on the expression of the 82 genes, two Prolif-like T cell-related GBM subtypes (C1 and C2) were constructed, with C1 exhibiting stronger proliferative activity. Survival models and scRNA-seq identified TK1 as a key gene associated with Prolif-like T cells in GBM. Further studies revealed that TK1 promotes GBM progression by influencing cell cycle and EMT processes, and targeting TK1 inhibition suppresses GBM proliferation and migration. Conclusions: TK1, as a Prolif-like T cell-associated marker, promotes GBM progression and can serve as a potential therapeutic target for GBM.
Keywords: Glioblastoma, Thymidine kinase 1, Prolif-like T cell, ScRNA-seq, stRNA-seq
Received: 29 Jun 2025; Accepted: 25 Aug 2025.
Copyright: © 2025 Deng, Chang and Shang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Wei Shang, First Affiliated Hospital, Dalian Medical University, Dalian, China
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