Evidence map›Paper›PMID 32255563›Full record

ArticleThe Kaohsiung journal of medical sciences2020

Knockdown of ubiquitin-specific peptidase 13 inhibits cell growth of hepatocellular carcinoma by reducing c-Myc expression.

Jing Huang, Zhen-Lin Gu, Wei Chen, Ying-Ying Xu, Ming Chen

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025
    Review
  5. Article
  6. Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023
    Review
  7. RNA splicing: a dual-edged sword for hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2022
    Review
  8. Role of USP13 in physiology and diseases.Frontiers in molecular biosciences · 2022
    Review
  9. USP13: Multiple Functions and Target Inhibition.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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

5 authors at 2 institutions in 1 country.

Jing HuangDepartment of Radiation Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Zhen-Lin GuDepartment of Interventional Radiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Wei ChenDepartment of Interventional Radiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Ying-Ying XuDepartment of Radiotherapy, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Ming ChenDepartment of Radiation Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID https://orcid.org/0000-0002-6114-1750
Xuzhou Medical College · CNSoochow University · CN

Funding

The Science and Technology Development funding of Nanjing Medical University NMUB2019358
6 · The paper itself

Abstract

Ubiquitin-specific peptidase 13 (USP13) has been reported to be involved in the tumorigenesis of several tumors, but its function in tumors is still controversial. In this study, the function of USP13 in hepatocellular carcinoma (HCC) was investigated, and we found that USP13 was significantly upregulated in both of primary HCC tumor tissues and cell lines. And HCC patients with high USP13 expression had a shorter overall survival or relapse-free survival than patients with low USP13 expression. In HCC cell lines, knockdown of USP13 by shRNAs markedly decreased HCC cell growth, and mechanistic investigations revealed that USP13 knockdown could markedly downregulate the expression levels of c-Myc. Moreover, overexpression of c-Myc could significantly attenuate the effects of shUSP13 on HCC cell growth inhibition. In addition, in vivo experiments showed that knockdown of USP13 could significantly inhibit xenograft tumor growth of HCC. Taken together, our present study provided the first evidence that USP13 acted as a novel driver in HCC tumorigenesis by regulating c-Myc expression, and targeting USP13 could be a promising strategy for HCC therapy.

Indexed as

Gene Expression Regulation, NeoplasticGene Knockdown TechniquesAnimalsCarcinoma, HepatocellularCell Line, TumorCell ProliferationHumansLiver NeoplasmsMice, NudeProto-Oncogene Proteins c-mycUbiquitin-Specific ProteasesProto-Oncogene Proteins c-mycUbiquitin-Specific ProteasesUSP13 protein, humancell growthc-MycHCCtargetUSP13

Identifiers

PMID32255563
PMCPMC11896304
OpenAlexW3015052255

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.