FLT3 expression and immune-associated transcriptional signatures in prostate cancer
- 1Department of Urology, The Affiliated Hospital of Xuzhou Medical University
Abstract
Background: Bulk transcriptomic profiles combine signals from malignant, stromal, and immune cells. This study examined immune-associated gene expression in prostate cancer using bulk and single-cell transcriptomic data, and separately assessed the effects of FLT3 knockdown in prostate cancer cell lines.
Methods: We screened 502 sample records from 497 patients and identified genes shared by ImmuneScore-associated differential expression and a weighted gene co-expression network module. Candidate genes were compared with four functional gene sets. We analyzed associations between FLT3 expression and immune-related signatures, examined single-cell expression patterns, and assessed FLT3 knockdown using two independent siRNAs in DU145 and 22Rv1 cells.
Results: The screening identified 64 shared genes, and comparison with the functional gene sets prioritized FLT3 and AIM2. FLT3 expression was associated with several immune-cell signatures; associations were stronger for total T-cell and B-cell signatures than for the CD8-positive T-cell signature. Single-cell analyses suggested FLT3 expression in cells annotated as monocytes. In DU145 and 22Rv1 cells, both FLT3-targeting siRNAs reduced growth and colony formation, reduced Transwell migration and invasion readouts, and altered epithelial–mesenchymal transition markers.
Conclusion: The tissue analyses support an association between FLT3 expression and immune-related transcriptional signals. The cell-line findings describe a separate in vitro phenotype and do not establish how FLT3 relates to lymphocyte infiltration. These findings do not establish a causal immune-regulatory mechanism or prognostic utility.
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BibTeX
@article{cui2026flt3,
title = {{FLT3 expression and immune-associated transcriptional signatures in prostate cancer}},
author = {Yongqiang Cui and Tianmou Song and Xingyue Wang and Zijin Wan and Lijun Mao},
journal = {Frontiers in Oncology},
year = {2026},
month = oct,
doi = {10.3389/fonc.2026.1970520},
url = {https://www.frontiersin.org/articles/10.3389/fonc.2026.1970520/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - FLT3 expression and immune-associated transcriptional signatures in prostate cancer
AU - Yongqiang Cui
AU - Tianmou Song
AU - Xingyue Wang
AU - Zijin Wan
AU - Lijun Mao
PY - 2026
DA - 2026/10/23
JO - Frontiers in Oncology
DO - 10.3389/fonc.2026.1970520
UR - https://www.frontiersin.org/articles/10.3389/fonc.2026.1970520/full
AB - Background: Bulk transcriptomic profiles combine signals from malignant, stromal, and immune cells. This study examined immune-associated gene expression in prostate cancer using bulk and single-cell transcriptomic data, and separately assessed the effects of FLT3 knockdown in prostate cancer cell lines. Methods: We screened 502 sample records from 497 patients and identified genes shared by ImmuneScore-associated differential expression and a weighted gene co-expression network module. Candidate genes were compared with four functional gene sets. We analyzed associations between FLT3 expression and immune-related signatures, examined single-cell expression patterns, and assessed FLT3 knockdown using two independent siRNAs in DU145 and 22Rv1 cells. Results: The screening identified 64 shared genes, and comparison with the functional gene sets prioritized FLT3 and AIM2. FLT3 expression was associated with several immune-cell signatures; associations were stronger for total T-cell and B-cell signatures than for the CD8-positive T-cell signature. Single-cell analyses suggested FLT3 expression in cells annotated as monocytes. In DU145 and 22Rv1 cells, both FLT3-targeting siRNAs reduced growth and colony formation, reduced Transwell migration and invasion readouts, and altered epithelial–mesenchymal transition markers. Conclusion: The tissue analyses support an association between FLT3 expression and immune-related transcriptional signals. The cell-line findings describe a separate in vitro phenotype and do not establish how FLT3 relates to lymphocyte infiltration. These findings do not establish a causal immune-regulatory mechanism or prognostic utility.
SN - 2234-943X
ER -