Evidence map›Paper›PMID 26568301›Full record

ArticleOncogene2016

Variants of ubiquitin-specific peptidase 24 play a crucial role in lung cancer malignancy.

Y-C Wang, S-A Wang, P-H Chen, T-I Hsu, W-B Yang, Y-P Chuang, W-C Su, H-J Liaw, W-C Chang, J-J Hung

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Impact ofInternational journal of molecular medicine · 2022
    Article
  11. USP24 promotes drug resistance during cancer therapy.Cell death and differentiation · 2021
    Article
  12. Article
  13. Article
  14. TheAutophagy · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Review
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

10 authors at 3 institutions in 1 country.

Y-C WangInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
S-A WangInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
P-H ChenDepartment of Pharmacology, National Cheng Kung University, Tainan, Taiwan.
T-I HsuInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
W-B YangInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Y-P ChuangDepartment of Pharmacology, National Cheng Kung University, Tainan, Taiwan.
W-C SuDepartment of Internal Medicine, College of Medicine and Hospital, National Cheng Kung University, Tainan, Taiwan.
H-J LiawDepartment of Life Science, College of Bioscience in Biotechnology, National Cheng Kung University, Tainan, Taiwan.
W-C ChangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
J-J HungInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TWTaipei Medical University · TWNational Cheng Kung University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin is a critical modifier regulating the degradation and function of its target proteins during posttranslational modification. Here we found that ubiquitin-specific peptidase 24 (USP24) is highly expressed in cell lines with enhanced malignancy and in late-stage lung cancer clinical samples. Studying single-nucleotide polymorphisms (SNPs) of USP24 using genomic DNA of lung cancer patients revealed an increase in SNP 7656C/T. When using RNA specimens instead of the genomic DNA of lung cancer patients, we found significant increases in the ratios of variants 930C/T and 7656T/C, suggesting that variants at these two sites are not only caused by the SNP of DNA but also by the RNA editing. USP24-930T and USP24-7656C increase USP24 expression levels by increasing RNA stability. Knocking down USP24 increased Suv39h1 level through a decrease in mouse double-minute 2 homolog levels, thus enhancing lysine-9 methylation of histone H3, and resulting in the prevention of lung cancer malignancy. In conclusion, as USP24 variant analysis revealed a higher ratio of variants in blood specimens of lung cancer patients than that in normal individuals, USP24-930T and USP24-7656C might be useful as diagnostic markers for cancer detection.

Indexed as

Polymorphism, Single NucleotideA549 CellsAnimalsBiomarkers, TumorBlotting, WesternCell Line, TumorGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenotypeHumansImmunohistochemistryLung NeoplasmsMaleMethyltransferasesMice, Inbred BALB CMice, NudeBiomarkers, TumorMDM2 protein, humanMethyltransferasesProto-Oncogene Proteins c-mdm2Repressor ProteinsSUV39H1 protein, humanUbiquitin ThiolesteraseUSP24 protein, human

Identifiers

PMID26568301
OpenAlexW2337700914

What Socratic holds

Textmetadata
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 Socratic graph.