Evidence map›Paper›PMID 27856536›Full record

ArticleEMBO reports2017

GRWD1 negatively regulates p53 via the RPL11-MDM2 pathway and promotes tumorigenesis.

Kota Kayama, Shinya Watanabe, Takuya Takafuji, Takahiro Tsuji, Kensuke Hironaka, Masaki Matsumoto, Keiichi I Nakayama, Masato Enari, Takashi Kohno, Kouya Shiraishi and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. GRWD1 Drives Melanoma Growth Through NF-κB Signaling Pathway.Dermatology practical & conceptual · 2025
    Article
  6. Article
  7. Article
  8. The Genetic Architecture of Congenital Diarrhea and Enteropathy.The New England journal of medicine · 2025
    Article
  9. Article
  10. Article
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  15. Article
  16. Article
  17. Review
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  19. Article
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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

14 authors at 2 institutions in 1 country.

Kota KayamaDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Shinya WatanabeDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Takuya TakafujiDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Takahiro TsujiDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Kensuke HironakaDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Masaki MatsumotoDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Keiichi I NakayamaDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Masato EnariDivision of Refractory and Advancer Cancer, National Cancer Center Research Institute, Tokyo, Japan.
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.
Kouya ShiraishiDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.
Tohru KiyonoDivision of Carcinogenesis and Cancer Prevention, National Cancer Center Research Institute, Tokyo, Japan.
Kazumasa YoshidaDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Nozomi SugimotoDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Masatoshi FujitaDepartment of Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan mfujita@phar.kyushu-u.ac.jp.ORCID 0000-0001-6617-2452
Kyushu University · JPGenesis Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ribosomal protein L11 (RPL11) binds and inhibits the MDM2 ubiquitin ligase, thereby promoting p53 stability. Thus, RPL11 acts as a tumor suppressor. Here, we show that GRWD1 (glutamate-rich WD40 repeat containing 1) physically and functionally interacts with RPL11. GRWD1 is localized to nucleoli and is released into the nucleoplasm upon nucleolar stress. Silencing of GRWD1 increases p53 induction by nucleolar stress, whereas overexpression of GRWD1 reduces p53 induction. Furthermore, GRWD1 overexpression competitively inhibits the RPL11-MDM2 interaction and alleviates RPL11-mediated suppression of MDM2 ubiquitin ligase activity toward p53. These effects are mediated by the N-terminal region of GRWD1, including the acidic domain. Finally, we show that GRWD1 overexpression in combination with HPV16 E7 and activated KRAS confers anchorage-independent growth and tumorigenic capacity on normal human fibroblasts. Consistent with this, GRWD1 overexpression is associated with poor prognosis in cancer patients. Taken together, our results suggest that GRWD1 is a novel negative regulator of p53 and a potential oncogene.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAnimalsCarrier ProteinsCell Line, TumorCell Transformation, NeoplasticCell Transformation, ViralDisease Models, AnimalFemaleGene ExpressionGene SilencingGenes, rasHeterograftsHumansMiceNeoplasmsCarrier ProteinsGRWD1 protein, humanProto-Oncogene Proteins c-mdm2ribosomal protein L11Ribosomal ProteinsTumor Suppressor Protein p53GRWD1nucleolar stressp53/RPL11tumorigenesis

Identifiers

PMID27856536
PMCPMC5210153
OpenAlexW2550207252

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.