Evidence map›Paper›PMID 29379164›Full record

ArticleOncogene2018

TRIM25 enhances cell growth and cell survival by modulating p53 signals via interaction with G3BP2 in prostate cancer.

Ken-Ichi Takayama, Takashi Suzuki, Tomoaki Tanaka, Tetsuya Fujimura, Satoru Takahashi, Tomohiko Urano, Kazuhiro Ikeda, Satoshi Inoue

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.6field-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

67 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025
    Review
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  12. Article
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7 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

8 authors at 7 institutions in 1 country.

Ken-Ichi TakayamaDepartment of Functional Biogerontology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo, Japan.
Takashi SuzukiDepartment of Pathology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Tomoaki TanakaDepartment of Clinical Cell Biology and Division of Endocrinology and Metabolism, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.ORCID 0000-0002-9761-1750
Tetsuya FujimuraDepartment of Urology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Satoru TakahashiDepartment of Urology, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan.
Tomohiko UranoDepartment of Geriatric Medicine, International University of Health and Welfare, Narita, Chiba, Japan.
Kazuhiro IkedaDivision of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Hidaka, Saitama, Japan.
Satoshi InoueDepartment of Functional Biogerontology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo, Japan. sinoue@tmig.or.jp.
Tokyo Metropolitan Institute of Gerontology · JPChiba University · JPInternational University of Health and Welfare · JPNihon University · JPSaitama Medical University · JPThe University of Tokyo · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer growth is promoted by the gene regulatory action of androgen receptor (AR) and its downstream signals. The aberrant dysfunction of tumor suppressor p53 has an important role in the prognosis of cancer. We previously found that androgen treatments translocate p53 to the cytoplasm. The mechanism of this translocation depends on sumoylation of p53 by complex of SUMO E3 ligase RanBP2 with androgen-induced GTPase-activating protein-binding protein 2 (G3BP2). Here, we identified tripartite motif-containing protein 25 (TRIM25)/estrogen-responsive finger protein (Efp) as a novel interacting partner of G3BP2 protein complex. Then, we demonstrated that TRIM25 knockdown resulted in p53 downstream activation for cell cycle inhibition and apoptosis induction in LNCaP and 22Rv1 cells. In contrast, overexpression of TRIM25 promoted prostate cancer cell proliferation and inhibited apoptosis by docetaxel treatment in LNCaP cells. We observed that p53 activity was reduced by mechanism of G3BP2-mediated nuclear export in TRIM25-overexpressing prostate cancer cells. We also found TRIM25 is important for G3BP2/RanBP2-mediated p53 modification. Clinically, we newly demonstrated that TRIM25 is a prognostic factor for prostate cancer patients. Expression of TRIM25 is significantly associated with cytoplasmic p53 expression and G3BP2. Moreover, TRIM25 knockdown results in reduced tumor growth and increased p53 activity in the mouse xenograft model of prostate cancer. Thus, our findings show that overexpression of TRIM25 promoted prostate cancer cell proliferation and cell survival by modulating p53 nuclear export mechanism with G3BP2 interaction.

Indexed as

Cell ProliferationAdaptor Proteins, Signal TransducingAgedAnimalsCarrier ProteinsCell NucleusCells, CulturedCell SurvivalHEK293 CellsHumansMaleMiceMice, NudeMiddle AgedProstatic NeoplasmsProtein BindingAdaptor Proteins, Signal TransducingCarrier ProteinsG3BP2 protein, humanRNA-Binding ProteinsTP53 protein, humanTranscription FactorsTRIM25 protein, humanTripartite Motif ProteinsTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID29379164
OpenAlexW2790075396

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.