Evidence map›Paper›PMID 32294625›Full record

ArticleAging2020

USP22 promotes development of lung adenocarcinoma through ubiquitination and immunosuppression.

Bing Han, Yue Sun, Dongdong Yang, Huijuan Zhang, Steven Mo, Xuesong Chen, Hailing Lu, Xueyan Mao, Jing Hu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
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  7. Bioinformatic analysis of the role of USP22 expression in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2025
    Article
  8. Article
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  11. Review
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  18. Article
  19. Multi-omics analysis of mScientific reports · 2021
    Article
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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

9 authors at 4 institutions in 1 country.

Bing HanDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Yue SunDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Dongdong YangDepartment of Surgical Oncology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Huijuan ZhangDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Steven MoNanning Life-Ontology Biotechnology Co., Ltd., Nanning, Guangxi, China.
Xuesong ChenDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Hailing LuDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Xueyan MaoHenan University of Science and Technology, Luoyang, Henan, China.
Jing HuDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CNFourth Affiliated Hospital of Harbin Medical University · CNHenan University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitin-specific protease 22 (USP22) expresses highly in lung adenocarcinoma (LUAD), which are associated with poor overall survival (OS). Microarray processing was performed to determine gene expression profiling, in which it was found that knocking down USP22 resulted in abnormal expression of a large number of genes. Differentially expressed genes (DEGs)-based protein-protein interaction (PPI) network was organized into 9 functional modules. These functional modules participated significantly in protein modification-related biological process and were involved in cancer-related pathways. The network was constructed to describe the global regulation of USP22-TF/pivot-module-pathway. It suggested that knocking down USP22 may up-regulate the expression of UBC to promote the pathways of cell cycle and ubiquitin-mediated proteolysis in the development of LUAD. More than that, knocking down USP22 can up-regulate STAT1 to activate JAK1-STAT1-caspase pathway, and promote apoptosis of tumor cell. Receiver operating characteristic (ROC) curve analysis suggested that E2F3, H2AFX, TFAP2A, PITX1, IRF7, and FOXM1 may be the potential diagnosis biomarkers for LUAD. On the other hand, BRCA1, FOXM1 and TFAP2A may be prognostic biomarkers of LUAD. In conclusion, we constructed a global regulation network to show that USP22 may promote the development of LUAD through ubiquitination and immunosuppression.

Indexed as

Gene Expression Regulation, NeoplasticUp-RegulationAdenocarcinoma of LungBiomarkers, TumorCell Line, TumorGene Expression ProfilingHumansImmunosuppression TherapyLung NeoplasmsRNA, NeoplasmUbiquitin ThiolesteraseBiomarkers, TumorRNA, NeoplasmUbiquitin ThiolesteraseUsp22 protein, humanglobal regulation networklung adenocarcinomaSTAT1UBCUSP22

Identifiers

PMID32294625
PMCPMC7202522
OpenAlexW3015819256

What Socratic holds

Textmetadata
LicenceCC BY
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.