Knockdown of CSF1R molecules enhances the antitumor effects of CD8+ T lymphocytes in bladder cancer
Abstract Objective In this study, we preliminarily investigated the efffects of the colony stimulating factor 1 receptor (CSF1R) molecules on CD8+ T cells in bladder cancer (BLCA) and the underlying molecular mechanism. Methods The effects of CSF1R in CD8+ T cells on BLCA cell proliferation, migrati...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Springer
2025-07-01
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| Series: | Discover Oncology |
| Subjects: | |
| Online Access: | https://doi.org/10.1007/s12672-025-03244-1 |
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| Summary: | Abstract Objective In this study, we preliminarily investigated the efffects of the colony stimulating factor 1 receptor (CSF1R) molecules on CD8+ T cells in bladder cancer (BLCA) and the underlying molecular mechanism. Methods The effects of CSF1R in CD8+ T cells on BLCA cell proliferation, migration and, invasion were determined by cell-killing assay and transwell assays.For in vivo experiments, tumours tissues were divided into four portions: (1) histological staining, (2) flow cytometry detection, (3) mRNA gene sequencing analysis, and (4) qPCR validation. Information related to 161 bladder cancer patients with BLCA at Xiangya Hospital of Central South University from 2019 to 2023 was collected. The pathological tissues were subjected to immunofluorescence. By calculating the Jordon index, CD8+ T cells with CSF1R expression at or above 0.39-fold were included in the high-expression group. Results Knocking down of CSF1R in CD8+ T cells inhibited BLCA proliferation, migration, and invasion. Flow cytometry revealed that it could lead to increased infiltration of immune cells. mRNA sequencing, quantitative polymerase chain reaction (PCR) and Western blot (WB) results suggested that creatine kinase (Ckm) was significantly decreased after CSF1R knockdown. Conclusion Our study provides novel insights into the roles of CSF1R in BLCA progression and the underlying crosstalk between tumour metabolism and the immune microenvironment. |
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| ISSN: | 2730-6011 |