Evidence map›Paper›PMID 37882969›Full record

ArticleInternational urology and nephrology2024

Multi-omics analysis reveals critical metabolic regulators in bladder cancer.

Chengcheng Wei, Changqi Deng, Rui Dong, Yaxin Hou, Miao Wang, Liang Wang, Teng Hou, Zhaohui Chen

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Article in International urology and nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.3field-weighted citation impact, top 19% of its field
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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Signal integrator function of CXXC5 in Cancer.Cell communication and signaling : CCS · 2025
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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 at 4 institutions in 1 country.

Chengcheng Wei *Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Changqi Deng *Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Rui Dong *Department of Urology, Hanyang Hospital of Wuhan City, Wuhan, 430050, China.
Yaxin HouDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Miao WangDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Liang WangDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Teng HouDepartment of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. h1aiyan@hust.edu.cn.
Zhaohui ChenDepartment of Urology, South China Hospital, Medical School, Shenzhen University, Shenzhen, 518116, People's Republic of China. zhaohuichen@hust.edu.cn.
Huazhong University of Science and Technology · CNShenZhen People’s Hospital · CNUnion Hospital · CNWuhan Hankou Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe crosstalk between genomic alterations and metabolic dysregulation in bladder cancer is largely unknown. A deep understanding of the interactions between cancer drivers and cancer metabolic changes will provide novel opportunities for targeted therapeutic strategies.

methodsThree primary bladder cancer specimens with paired normal tissues or blood samples were subjected to whole-exome sequencing, DNA methylation array and whole-transcriptome sequencing by next-generation sequencing technology. We applied the methods to multi-omics data combining the Cancer Genome Atlas (TCGA) bladder cancer samples, including somatic mutation, DNA copy number, DNA methylation and gene expression profile for validation.

resultsWe identified 34 mutated cancer driver genes in bladder cancer. KDM6A was the most significantly mutated cancer driver gene. Metabolic pathways were enriched in both differentially methylated regions (DMRs) and differentially expressed genes. Twenty-nine DMRs in the TSS200 region were highly correlated with the upregulation of gene expression, and 24 DMRs in the genome were highly correlated with the downregulation of gene expression. A total of 201 genes had highly correlated DNA methylation and expression. Thirty-four genes, including the known metabolic genes CXXC5, PRR5, ABCB8 and BAHD1, were further validated in the TCGA cohort. Multi-omics alterations identified two new candidate driver genes, WIPI2 and GFM2, that warrant future studies.

conclusionsThis study provides a comprehensive and systematic analysis, focusing on identifying key regulatory factors that may lead to cancer metabolic heterogeneity. Further understanding and verification of the cancer genes driving metabolic reprogramming and their role in the progression of bladder cancer will help to identify new therapeutic targets.

Indexed as

MultiomicsUrinary Bladder NeoplasmsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDNA MethylationHumansTranscription FactorsTranscriptomeBAHD1 protein, humanChromosomal Proteins, Non-HistoneCXXC5 protein, humanDNA-Binding ProteinsTranscription FactorsBladder cancerCancer Genome Atlas (TCGA)MetabolismMulti-omicsRegulators

Identifiers

PMID37882969
OpenAlexW4387948812

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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.