Evidence map›Paper›PMID 32468271›Full record

ArticleInvestigational new drugs2020

Ubiquitin-specific protease 7 is a druggable target that is essential for pancreatic cancer growth and chemoresistance.

Hao Chen, Xiaoling Zhu, Rong Sun, Panpan Ma, Erhao Zhang, Zhou Wang, Yihui Fan, Guoxiong Zhou, Renfang Mao

Abstract read
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In one paragraph

Article in Investigational new drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. Unraveling the Predictive Value ofStem cells international · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. A review of deubiquitinases and thier roles in tumorigenesis and development.Frontiers in bioengineering and biotechnology · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. Review
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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 2 institutions in 1 country.

Hao ChenDepartment of Gastroenterology, Affiliated Hospital of Nantong University, 20 Xisi Road, 226001, Jiangsu, Nantong, China.
Xiaoling ZhuDepartment of Gastroenterology, Affiliated Hospital of Nantong University, 20 Xisi Road, 226001, Jiangsu, Nantong, China.
Rong SunLaboratory of Medical Science, School of Medicine, Nantong University, 226001, Jiangsu, China.
Panpan MaLaboratory of Medical Science, School of Medicine, Nantong University, 226001, Jiangsu, China.
Erhao ZhangLaboratory of Medical Science, School of Medicine, Nantong University, 226001, Jiangsu, China.
Zhou WangSchool of Life Sciences, Nantong University, 226001, Jiangsu, China.
Yihui FanLaboratory of Medical Science, School of Medicine, Nantong University, 226001, Jiangsu, China.
Guoxiong ZhouDepartment of Gastroenterology, Affiliated Hospital of Nantong University, 20 Xisi Road, 226001, Jiangsu, Nantong, China. Zhougx@ntu.edu.cn.
Renfang MaoLaboratory of Medical Science, School of Medicine, Nantong University, 226001, Jiangsu, China. maorenfang@ntu.edu.cn.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, and most patients die within one year after diagnosis. This cancer is resistant to almost all current therapies, so there is an urgent need to identify novel druggable targets. Ubiquitin-specific protease 7 (USP7) is a deubiquitinase that functions in carcinogenesis, but its role in PDAC is unknown. Our experiments indicated that several subtypes of PDAC cells are sensitive to USP7 inhibition. In particular, pharmaceutical inhibition of USP7 by the small molecule P22077 attenuated PDAC cell growth and induced cell death in vitro and in vivo. Pharmaceutical inhibition of USP7 in P22077-resistant PDAC cells allowed them to overcome chemoresistance. Genetic silencing experiments supported the importance of USP7 in the pathogenesis of PDAC. In particular, genetic disruption of USP7 greatly reduced cell proliferation and chemoresistance in vitro and prevented PDAC growth in vivo. Protein profiling by mass spectrometry (MS) indicated USP7 was associated 4 ontology terms: translation, localization and protein transporting, nucleotide or ribonucleotide binding, and ubiquitin-dependent catabolic processes. Puromycin labeling indicated that P22077 greatly reduced protein synthesis, and transcriptional analysis indicated that P22077 significantly altered the extracellular space matrix. In summary, we provided multiple lines of evidence which indicate that USP7 plays a critical role in PDAC, and may therefore be a suitable target for treatment of this cancer.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMice, NudePancreatic NeoplasmsThiophenesUbiquitin-Specific Peptidase 71-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanoneAntineoplastic AgentsThiophenesUbiquitin-Specific Peptidase 7chemoresistancePancreatic ductal adenocarcinomatranslationUSP7

Identifiers

PMID32468271
OpenAlexW3029591423

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.