Evidence map›Paper›PMID 31570706›Full record

ArticleCell death & disease2019

Ubiquitin ligase TRIM71 suppresses ovarian tumorigenesis by degrading mutant p53.

Yajie Chen, Qian Hao, Jieqiong Wang, Jiajia Li, Canhua Huang, Yu Zhang, Xiaohua Wu, Hua Lu, Xiang Zhou

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Multifaceted role ofMedComm · 2024
    Review
  6. Review
  7. Review
  8. SCFBiomedicines · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. The ARTS of p53-dependent mitochondrial apoptosis.Journal of molecular cell biology · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Inactivation of the tumor suppressor p53 by long noncoding RNA RMRP.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Review
  20. 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

9 authors at 6 institutions in 2 countries.

Yajie ChenCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
Qian HaoCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
Jieqiong WangCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
Jiajia LiDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Canhua HuangDepartment of Obstetrics and Gynecology, Xiangya Hospital, Central South University, Changsha, 410008, China.
Yu ZhangDepartment of Obstetrics and Gynecology, Xiangya Hospital, Central South University, Changsha, 410008, China.
Xiaohua WuDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Hua LuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA. hlu2@tulane.edu.
Xiang ZhouCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China. xiangzhou@fudan.edu.cn.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CNCentral South University · CNFudan University · CNTulane University · USXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hotspot p53 mutants augment cancer cell proliferation, metastasis and metabolism through their gain-of-function (GOF). Ovarian cancer sustains the highest frequency of TP53 mutations, but the mechanisms underlying regulation of mutant p53s' GOF in this type of cancer remain incompletely understood. Herein, we identified the E3-ubiquitin ligase TRIM71 as a novel mutant p53-binding protein. Ectopic TRIM71-induced ubiquitination and proteasomal degradation of mutant p53 by binding to its transactivation (TA) domain, and inhibited the expression of a broad spectrum of mutant p53 target genes. Ectopic TRIM71 also restrained, whereas ablation of TRIM71 endorsed, ovarian carcinoma cell growth in vitro and in vivo. Significantly, TRIM71 overexpression is highly associated with favorable prognosis, particularly, in TP53-mutated ovarian carcinomas. Altogether, our findings unveil the anti-tumor function of TRIM71 in ovarian cancer development and prognosis by downregulating mutant p53s.

Indexed as

AnimalsCarcinogenesisCell Line, TumorDatabases, GeneticFemaleGene Expression Regulation, NeoplasticHeterograftsHumansMaleMiceMutant ProteinsOvarian NeoplasmsProstatic NeoplasmsTripartite Motif ProteinsTumor Suppressor Protein p53UbiquitinationMutant ProteinsTP53 protein, humanTRIM71 protein, humanTripartite Motif ProteinsTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID31570706
PMCPMC6769007
OpenAlexW2975960572

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.