Evidence map›Paper›PMID 40026288›Full record

ReviewCancer medicine2025

Molecular Mechanisms of ARD1 in Tumors.

Chunjiao Yu, Hongtao Lei, Xuefei Hou, Shan Yan

Abstract readReview
In one paragraph

Review in Cancer medicine, 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

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

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

4 authors.

Chunjiao YuInstitute of Biomedical Engineering, Kunming Medical University, Chenggong District, Kunming, Yunnan, People's Republic of China.ORCID https://orcid.org/0009-0003-0931-6933
Hongtao LeiInstitute of Biomedical Engineering, Kunming Medical University, Chenggong District, Kunming, Yunnan, People's Republic of China.
Xuefei HouInstitute of Biomedical Engineering, Kunming Medical University, Chenggong District, Kunming, Yunnan, People's Republic of China.
Shan YanInstitute of Biomedical Engineering, Kunming Medical University, Chenggong District, Kunming, Yunnan, People's Republic of China.

Funding

National Natural Science Foundation of China 82260537National Natural Science Foundation of China 82460478
6 · The paper itself

Abstract

introductionArrest-deficient protein 1 (ARD1) is an acetyltransferase that acetylates the N-terminal amino acids and internal lysine residues of proteins. It plays a crucial role in various cellular processes. The significance of ARD1 in tumor development has become increasingly evident in recent years.

methodsThis review analyzes the regulatory role of ARD1 in tumor progression by examining its involvement in processes such as cell cycle regulation, cell proliferation, metastasis, apoptosis, and autophagy. Additionally, we discuss the expression patterns and molecular mechanisms of ARD1 in different types of cancer.

resultsElevated levels of ARD1 have been reported in several cancer types. Its increased expression is associated with various tumor characteristics, suggesting it may serve as a potential prognostic biomarker. Furthermore, ARD1 could be targeted for the development of novel cancer therapies.

conclusionUnderstanding the role of ARD1 in tumor biology provides valuable insights into potential therapeutic targets and biomarkers for cancer treatment. This review highlights the advances in ARD1-related research and suggests that it may be a promising avenue for improving cancer prognosis and treatment strategies.

Indexed as

NeoplasmsN-Terminal Acetyltransferase EAnimalsApoptosisAutophagyBiomarkers, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansN-Terminal Acetyltransferase APrognosisBiomarkers, TumorNAA10 protein, humanN-Terminal Acetyltransferase AN-Terminal Acetyltransferase EacetylationARD1tumor

Identifiers

PMID40026288
PMCPMC11873779

What OpenQuestion holds

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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.