Evidence map›Paper›PMID 41858347›Full record

ArticleFrontiers in oncology2026

Peroxisomal activity drives aggressive bladder cancer phenotypes and reveals erythorbic acid as a potential therapeutic modulator.

Qinghui Wu, Yu Zhou, Zhewen Ou, Housheng Fu, Fanchang Zeng, Daoyuan Li, Zhaocong Zheng, Fei Wang

Abstract read
In one paragraph

Article in Frontiers in 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.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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

8 authors.

Qinghui WuDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.
Yu ZhouAdmission Service Center, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.
Zhewen OuDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.
Housheng FuDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.
Fanchang ZengDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.
Daoyuan LiDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.
Zhaocong ZhengDepartment of Radiation Oncology, Guangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, China.
Fei WangDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Provincial Clinical Medical Center, Haikou, Hainan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Peroxisomes play essential roles in cellular lipid metabolism and redox regulation, yet their contribution to bladder cancer (BLCA) progression remains poorly defined. Methods: Transcriptomic and clinical data from TCGA-BLCA and three GEO cohorts were integrated to identify prognostic peroxisome-related genes (PRGs). A six-gene PRG signature was constructed and validated for survival prediction, molecular subtype stratification, and pathway enrichment analyses, with expression validation in bladder cancer cell lines. Drug-gene enrichment and molecular docking were then performed to identify potential therapeutic modulators, which were subsequently assessed using CCK-8 cell viability assays. Results: Two distinct PRG-based molecular subtypes of BLCA were identified, showing significant differences in survival, mutational landscape, immune infiltration, and metabolic signaling. The high-risk subtype was enriched for PRDX1, ACOX2, and IDI1, reflecting enhanced oxidative stress adaptation and metabolic reprogramming, while the low-risk group was defined by ACSL5 and XDH. Drug-gene enrichment identified erythorbic acid, a redox-active ascorbate analog, as the most biologically relevant compound targeting high-risk PRGs. Molecular docking confirmed stable binding of erythorbic acid to ACOX2 (-6.2 kcal/mol), IDI1 (-6.6 kcal/mol), and PRDX1 (-5.4 kcal/mol) within catalytically active pockets, suggesting coordinated modulation of oxidative metabolism and redox balance. Subsequent CCK-8 assays demonstrated a dose- and time-dependent reduction in viability in bladder cancer cell lines. In contrast, normal urothelial XV-HUC-1 cells showed relatively preserved viability, indicating differential cellular responses to erythorbic acid Conclusion: Peroxisome-related gene dysregulation shapes the metabolic and immunologic heterogeneity of bladder cancer. Erythorbic acid emerges as a promising redox-metabolic modulator targeting multiple peroxisomal enzymes, offering a potential therapeutic avenue for aggressive, high-risk BLCA subtypes.

Indexed as

bladder cancer (BC)cancer metabolismperoxisomesstromal cellstumor microenvironment (TME)

Identifiers

PMID41858347
PMCPMC12995624

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.