Evidence map›Paper›PMID 25146927›Full record

ArticleCell death and differentiation2014

E3 ubiquitin ligase TRIM32 negatively regulates tumor suppressor p53 to promote tumorigenesis.

Ju Liu, C Zhang, X L Wang, P Ly, V Belyi, Z Y Xu-Monette, K H Young, W Hu, Z Feng

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

96 citing papers in PubMed, 136 citations in OpenAlex.

  1. Trial
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  10. Targeting the 3D genome by anthracyclines for chemotherapeutic effects.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  18. iScience · 2024
    Article
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36 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Ju LiuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA.
C ZhangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA.
X L Wang1] Department of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA [2] Department of Breast Surgery, Qilu Hospital, Shandong University, Ji'nan, China.
P LyDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA.
V BelyiCenter for Systems Biology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA.
Z Y Xu-MonetteDepartment of Hematopathology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
K H YoungDepartment of Hematopathology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
W HuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA.
Z FengDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, State University of New Jersey, New Brunswick, NJ, USA.
Rutgers Cancer Institute of New JerseyRutgers, The State University of New Jersey · USThe University of Texas MD Anderson Cancer Center · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
The Role of LIF, a Novel Negative Regulator of p53, in Colorectal CancerR01CA160558 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HU, WENWEI · 2012 to 2017
$1.6M
The role of glutaminase 2, a novel p53 target gene in metabolism, in liver cancerR01CA143204 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI FENG, ZHAOHUI · 2010 to 2014
$1.6M
NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA143204NCI NIH HHS R01CA143204NCI NIH HHS R01 CA160558NCI NIH HHS R01CA160558
6 · The paper itself

Abstract

Tumor suppressor p53 has a key role in maintaining genomic stability and preventing tumorigenesis through its regulation of cellular stress responses, including apoptosis, cell cycle arrest and senescence. To ensure its proper levels and functions in cells, p53 is tightly regulated mainly through post-translational modifications, such as ubiquitination. Here, we identified E3 ubiquitin ligase TRIM32 as a novel p53 target gene and negative regulator to regulate p53-mediated stress responses. In response to stress, such as DNA damage, p53 binds to the p53 responsive element in the promoter of the TRIM32 gene and transcriptionally induces the expression of TRIM32 in cells. In turn, TRIM32 interacts with p53 and promotes p53 degradation through ubiquitination. Thus, TRIM32 negatively regulates p53-mediated apoptosis, cell cycle arrest and senescence in response to stress. TRIM32 is frequently overexpressed in different types of human tumors. TRIM32 overexpression promotes cell oncogenic transformation and tumorigenesis in mice in a largely p53-dependent manner. Taken together, our results demonstrated that as a novel p53 target and a novel negative regulator for p53, TRIM32 has an important role in regulation of p53 and p53-mediated cellular stress responses. Furthermore, our results also revealed that impairing p53 function is a novel mechanism for TRIM32 in tumorigenesis.

Indexed as

AnimalsApoptosisCell Line, TumorCell Transformation, NeoplasticDNA DamageHumansMiceTranscription FactorsTripartite Motif ProteinsTumor Suppressor Protein p53UbiquitinationUbiquitin-Protein LigasesTranscription FactorsTRIM32 protein, humanTripartite Motif ProteinsTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID25146927
PMCPMC4211364
OpenAlexW1972798599

What OpenQuestion holds

Textmetadata
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.