Evidence map›Paper›PMID 42055487›Full record

ArticleTranslational oncology2026

Integrative multi-omics analysis identifies key ubiquitination regulators in prostate cancer.

Hairong Wei, Chen Gong, Zhiyong Tan, Engui Yang, Yinglong Huang, Ye An, Haihao Li, Dihao Lv, Chadanfeng Yang, Wujie Chen and 4 more

Abstract read
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In one paragraph

Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Hairong WeiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Chen GongDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China; Department of Urology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan, China.
Zhiyong TanDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Engui YangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Yinglong HuangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Ye AnDepartment of Urology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan, China.
Haihao LiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Dihao LvDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Chadanfeng YangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Wujie ChenDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Haifeng WangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China.
Senmao LiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China. Electronic address: lisenmao@kmmu.edu.cn.
Mingxia DingDepartment of Urology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan, China. Electronic address: dingmingxia@kmmu.edu.cn.
Jiansong WangDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, Yunnan, China; Kunming Medical University, Kunming, 650500, Yunnan, China. Electronic address: wangjiansong@kmmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUbiquitination plays a crucial role in tumor regulation, yet its specific functions in prostate cancer (PCa) remain incompletely understood. This study aimed to identify key genes associated with ubiquitination processes in PCa and validate their roles across multiple biological levels.

methodsWe integrated single-cell RNA sequencing (scRNA-seq) data from the GEO database with summary-level genome-wide association study (GWAS) data. Through differential expression analysis, summary data-based Mendelian randomization (SMR), and single-cell trajectory analysis, ubiquitination-related genes (URGs) associated with PCa were screened. Validation was performed at both tissue and cellular levels: immunohistochemistry (IHC) on 30 PCa tissue samples stratified by Gleason grade (low-grade: ≤ 3 + 4; high-grade: ≥ 4 + 3), and Western blot (WB) along with quantitative PCR (qPCR) on PCa cell lines (22Rv1, LNCaP, PC-3) versus a normal prostate epithelial cell line (RWPE-1). Functional experiments including Transwell migration, wound healing, CCK-8 proliferation assays, and a cell line-derived xenograft (CDX) mouse model were conducted to validate the biological function of TRIM8.

resultsT lymphocytes and epithelial cells were the predominant cell types in the PCa microenvironment. SMR and MR analyses identified POLI and TRIM8 as key causal genes with significant protective associations against PCa (POLI: OR = 0.9385, P = 0.0046; TRIM8: OR = 0.8648, P < 0.001). Colocalization analyses supported their genetic regulatory roles. Molecular docking indicated a high binding affinity between selegiline hydrochloride and POLI (ΔG = -11.3kcal/mol). Experimental validations confirmed these findings: IHC revealed elevated POLI expression in high-grade tumors and higher TRIM8 expression in low-grade tumors. Consistently, WB and qPCR analyses demonstrated that POLI was significantly upregulated, while TRIM8 was downregulated, in PCa cell lines compared to normal controls. Functional assays further demonstrated that TRIM8 overexpression suppressed PC-3 cell migration, proliferation, and in vivo tumor growth, whereas TRIM8 knockdown exerted opposite effects, confirming its tumor-suppressive role.

conclusionsPOLI and TRIM8 are key ubiquitination regulators with causal links to PCa pathogenesis, exhibiting distinct expression patterns correlated with tumor aggressiveness. Functional validation confirms TRIM8 as a tumor suppressor in PCa. These genes represent promising therapeutic targets, and the predicted interaction with selegiline hydrochloride highlights a potential drug-repurposing strategy.

Indexed as

Mendelian randomizationProstate cancerSingle-cell RNA sequencingSummary data-based mendelian randomizationUbiquitination

Identifiers

PMID42055487
PMCPMC13141746

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