Evidence map›Paper›PMID 41347086›Full record

ArticleFrontiers in oncology2025

Pan-cancer landscape of UBD/FAT10 and experimental validation in esophageal carcinoma.

Xu Zhang, Hongnian Pan, Xiuzhong Wang

Abstract read
In one paragraph

Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
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

3 authors.

Xu ZhangDepartment of Gastroenterology, Lu'an Hospital of Anhui Medical University, Lu'an, China.
Hongnian PanDepartment of Gastroenterology, Lu'an Hospital of Anhui Medical University, Lu'an, China.
Xiuzhong WangDepartment of Gastroenterology, Lu'an Hospital of Anhui Medical University, Lu'an, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To comprehensively characterize the pan-cancer roles of Ubiquitin D (UBD/FAT10) in tumorigenesis, immune regulation, and therapeutic response through integrative multi-omics and expe+rimental analyses. Methods: Utilizing bulk RNA-seq (TCGA/GTEx/CPTAC), immune deconvolution, proteomics, and functional enrichment, we analyzed UBD expression, survival prognosis, immune infiltration, and molecular pathways across 33 cancers. Molecular docking and MD simulations were performed to assess UBD-protein interactions. Through lentivirus-mediated overexpression, functional assays (CCK-8, colony formation, wound healing, and Transwell), transcriptome sequencing, and biochemical validation, we demonstrated that UBD promotes malignant phenotypes in esophageal cancer via the TP53 signaling pathway. Results: UBD was upregulated in 14 cancers but downregulated in thyroid carcinoma (THCA) and kidney chromophobe (KICH). ROC analysis highlighted UBD's diagnostic potential (AUC >0.8 in gastrointestinal tumors). High UBD conferred protection in melanoma (SKCM, HR = 0.891) and sarcoma (SARC, HR = 0.899) but predicted poor outcomes in uveal melanoma (UVM, HR = 1.298) and pancreatic adenocarcinoma (PAAD, HR = 1.143).UBD positively correlated with the IFN-γ-dominant immune subtype (C2), characterized by CD8+ T cells/M1 macrophages. Drug sensitivity profiling nominated imatinib (Vina score: -8.9 kcal/mol) and TTNPB as potential therapies for UBD-high tumors, validated by stable MD simulations. In esophageal carcinoma (ESCA), UBD expression escalated with tumor stage and predicted poor survival (p<0.05).UBD enhances the proliferation and migration of esophageal cancer cells by modulating the TP53 signaling pathway, as validated through transcriptomic analysis and functional assays. Conclusions: This study advances UBD as a prognostic indicator and therapeutic target, bridging molecular insights with clinical translation in precision oncology.

Indexed as

cancerimmunepan cancerTCGAubiquitin D

Identifiers

PMID41347086
PMCPMC12672329

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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.