ORIGINAL RESEARCH article
Front. Immunol.
Sec. B Cell Biology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1606607
Mitogen-activated protein kinase pathway and four genes involved in the development of benign prostatic hyperplasia: in vivo and vitro validation
Provisionally accepted
- 1Wuhan University, Wuhan, China
- 2Zhongnan Hospital, Wuhan University, Wuhan, Hubei Province, China
- 3wuhan sec, wuhan, China
- 4Henan University, Kaifeng, Henan Province, China
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Background: Benign prostatic hyperplasia (BPH) is a common age-associated disorder characterized by nonmalignant proliferation of prostate tissues. However, its underlying molecular mechanisms remain incompletely elucidated.Methods: A rat model of BPH was established via surgical castration followed by testosterone propionate administration. Proteomic profiling was performed on prostate tissues from BPH and sham-operated rats. Public datasets of BPH patients and healthy individuals were also analyzed to validate the translational relevance. In addition, qPCR was conducted on both rat tissues and human-derived prostate cell lines to confirm gene expression levels. Furthermore, immunohistochemistry was performed on prostate tissue samples from BPH patients to examine the expression and localization of the target proteins.Results: Proteomic analysis revealed significant upregulation of four proteins-QPCT, ARHGEF37, FLNC, and LGALS7-in BPH model rats compared to controls. KEGG pathway enrichment identified the MAPK signaling pathway as a potential key regulator of BPH progression. Similar expression patterns were observed in human datasets. qPCR results further validated the elevated expression of these four proteins in both rat and human BPH-related samples. Immunohistochemistry further demonstrated that all four proteins were highly expressed in prostate tissues from BPH patients.The aberrant overexpression of QPCT, ARHGEF37, FLNC, and LGALS7, along with dysregulation of the MAPK signaling pathway, may contribute to BPH pathogenesis. These findings provide new insights into the molecular mechanisms of BPH and may inform the development of diagnostic markers or therapeutic targets.
Keywords: Benign prostatic hyperplasia, Proteomics, MAPK pathway, Genetic Markers, immunology
Received: 05 Apr 2025; Accepted: 21 Oct 2025.
Copyright: © 2025 JIAMIN, guo, Wu, Li, Deng, wang and Zeng. 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: GU JIAMIN, g378527624@163.com
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