Evidence map›Paper›PMID 36186123›Full record

ArticleAging and disease2022

UPP1 Promotes Lung Adenocarcinoma Progression through Epigenetic Regulation of Glycolysis.

Xuan Wang, Zheng Wang, Renhong Huang, Zhouyi Lu, Xiaofeng Chen, Dayu Huang

Abstract read
In one paragraph

Article in Aging and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  14. Uridine as a hub in cancer metabolism and RNA biology.Experimental & molecular medicine · 2025
    Review
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  19. The Role of Uridine in Health and Disease.Journal of inflammation research · 2025
    Review
  20. A potential XGBoost Diagnostic Score forFrontiers in immunology · 2025
    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

6 authors.

Xuan Wang *1Department of Thoracic Surgery Huashan Hospital & Cancer Metastasis Institute, Fudan University, Shanghai 200040, China.
Zheng Wang *2Department of General Surgery, Comprehensive Breast Health Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Renhong Huang *2Department of General Surgery, Comprehensive Breast Health Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Zhouyi Lu1Department of Thoracic Surgery Huashan Hospital & Cancer Metastasis Institute, Fudan University, Shanghai 200040, China.
Xiaofeng Chen1Department of Thoracic Surgery Huashan Hospital & Cancer Metastasis Institute, Fudan University, Shanghai 200040, China.
Dayu Huang1Department of Thoracic Surgery Huashan Hospital & Cancer Metastasis Institute, Fudan University, Shanghai 200040, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uridine phosphorylase 1 (UPP1) is a dimeric enzyme that plays an indispensable role in pyrimidine salvage as well as uridine homeostasis and is upregulated in various cancers, including LUAD. However, the function and underlying mechanisms of UPP1 in mediating LUAD cell progression are still largely unknown. Single-cell RNA transcription analysis was applied to compare the expression of UPP1 in tumor tissues and adjacent tissue. In vitro gain- and loss-of-function experiments with LUAD cells were performed to elucidate the functions of UPP1. Western blotting, qRT-PCR, cell apoptosis, IHC staining, Seahorse XF24 Extracellular Flux analysis, chromatin immunoprecipitation (ChIP) assay, and bioinformatics analysis were performed to reveal the underlying mechanisms. In this study, UPP1 was found to be the top metabolism-related gene that was upregulated by single-cell transcriptomic profiling of LUAD. Next, we confirmed that UPP1 was highly expressed in LUAD tissues and cell lines and was correlated with poor overall survival in LUAD patients. UPP1 drove glycolytic metabolism and significantly regulated the sensitivity of tumors to glycolytic inhibitors in vitro and in vivo. UPP1 is subject to epigenetic regulation through histone acetylation. The CBP/p300 inhibitor SGC-CBP30 reduced the protein levels of UPP1, H3K27ac, and H3K9ac. ChIP assays revealed that acetyl-histone H3 and RNA polymerase II bind to the UPP1 promoter. UPP1 overexpression restored lactic acid production and glucose uptake compared to the SGC-CBP30 group. Our findings confirm UPP1 as a novel oncogene in LUAD, thus providing a potential novel diagnostic and therapeutic target for LUAD.

Indexed as

epigenetic regulationglycolysislung adenocarcinomasingle-cell analysisUridine phosphorylase 1

Identifiers

PMID36186123
PMCPMC9466982

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Registered trials

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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.