Evidence map›Paper›PMID 31969492›Full record

ArticleAging2020

SENP1 is a crucial promotor for hepatocellular carcinoma through deSUMOylation of UBE2T.

Yifeng Tao, Ruidong Li, Conghuan Shen, Jianhua Li, Quanbao Zhang, Zhenyu Ma, Feifei Wang, Zhengxin Wang

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Naturally Derived SENP1 Inhibitors with Anticancer Activity.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Abnormal protein SUMOylation in liver disease: novel target for therapy.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

8 authors at 2 institutions in 1 country.

Yifeng TaoDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Ruidong LiDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Conghuan ShenDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Jianhua LiDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Quanbao ZhangDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Zhenyu MaDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Feifei WangBioscience Research Center, Shanghai 200120, China.
Zhengxin WangDepartment of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, China.
Huashan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cooperative roles of SENP1 and UBE2T in development and progression of hepatocellular carcinoma (HCC) are still unknown. The expression levels of SENP1 and UBE2T were evaluated in clinical specimens and HCC cells. The relationship between clinicopathological features and SENP1 were analyzed. We constructed the HepG2-SENP1 knockout cell model and explored the functions of SENP1 and UBE2T in HCC development. UBE2T was confirmed as a novel deSUMOylation target of SENP1. Upregulation of SENP1 and UBE2T were observed in HCC tissues and most hepatoma cell lines, and their expression levels were proved to be positively related. Knockout of SENP1 resulted in impaired growth, migration and invasion, and enhanced apoptosis in vitro, as well as inhibition of tumor growth in vivo. Furthermore, we demonstrated that SENP1 could directly deSUMOylate UBE2T thereby increasing its expression and activating Akt pathway. Functional studies showed that UBE2T overexpression or K8R mutation promoted cell growth, migration and invasion. In conclusion, our study demonstrated that SENP1 and UBE2T were positively related and functioned as tumor promoters. The carcinogenesis of SENP1 is mediated by deSUMOylation of UBE2T and the UBE2T/Akt pathway. Notably, UBE2T was identified as a novel deSUMOylation target of SENP1 in this study for the first time.

Indexed as

Amino Acid SequenceApoptosisCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCell ProliferationCysteine EndopeptidasesFemaleGene ExpressionGene Knockdown TechniquesGene Knockout TechniquesHumansLiver NeoplasmsMaleModels, BiologicalCysteine EndopeptidasesSENP1 protein, humanUBE2T protein, humanUbiquitin-Conjugating EnzymesAktdeSUMOylationhepatocellular carcinomaSENP1UBE2T

Identifiers

PMID31969492
PMCPMC7053586
OpenAlexW3002163920

What OpenQuestion 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 OpenQuestion graph.