Evidence map›Paper›PMID 32108164›Full record

ArticleOncogene2020

Cancer-associated mutations in the ribosomal protein L5 gene dysregulate the HDM2/p53-mediated ribosome biogenesis checkpoint.

Ines Oršolić, Slađana Bursać, Deana Jurada, Irena Drmić Hofman, Zlatko Dembić, Jiri Bartek, Ivana Mihalek, Siniša Volarević

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-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

39 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. RiboScreenBiomedicines · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Ribosome specialization by cancer-associated ribosomal protein mutations: progress made and open questions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Ribosome heterogeneity in development and disease.Frontiers in cell and developmental biology · 2024
    Article
  17. Article
  18. Article
  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 4 institutions in 4 countries.

Ines OršolićDepartment of Molecular Medicine and Biotechnology, University of Rijeka, Faculty of Medicine, Rijeka, 51000, Croatia.
Slađana BursaćDepartment of Molecular Medicine and Biotechnology, University of Rijeka, Faculty of Medicine, Rijeka, 51000, Croatia.
Deana JuradaDepartment of Molecular Medicine and Biotechnology, University of Rijeka, Faculty of Medicine, Rijeka, 51000, Croatia.
Irena Drmić HofmanDepartment of Medical Chemistry and Biochemistry, University of Split, School of Medicine, Split, 21000, Croatia.
Zlatko DembićInstitute for Oral Biology, Faculty of Dentistry, University of Oslo, PB 1052 Blindern, Oslo, N0316, Norway.ORCID http://orcid.org/0000-0002-9970-6497
Jiri BartekDivision of Genome Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, 17176, Stockholm, Sweden. jb@cancer.dk.
Ivana MihalekDepartment of Molecular Medicine and Biotechnology, University of Rijeka, Faculty of Medicine, Rijeka, 51000, Croatia. ivana.mihalek@medri.uniri.hr.
Siniša VolarevićDepartment of Molecular Medicine and Biotechnology, University of Rijeka, Faculty of Medicine, Rijeka, 51000, Croatia. sinisa.volarevic@medri.uniri.hr.
University of Rijeka · HRScience for Life Laboratory · SEUniversity of Oslo · NOUniversity of Split · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perturbations in ribosome biogenesis have been associated with cancer. Such aberrations activate p53 through the RPL5/RPL11/5S rRNA complex-mediated inhibition of HDM2. Studies using animal models have suggested that this signaling pathway might constitute an important anticancer barrier. To gain a deeper insight into this issue in humans, here we analyze somatic mutations in RPL5 and RPL11 coding regions, reported in The Cancer Genome Atlas and International Cancer Genome Consortium databases. Using a combined computational and statistical approach, complemented by a range of biochemical and functional analyses in human cancer cell models, we demonstrate the existence of several mechanisms by which RPL5 mutations may impair wild-type p53 upregulation and ribosome biogenesis. Unexpectedly, the same approach provides only modest evidence for a similar role of RPL11, suggesting that RPL5 represents a preferred target during human tumorigenesis in cancers with wild-type p53. Furthermore, we find that several functional cancer-associated RPL5 somatic mutations occur as rare germline variants in general population. Our results shed light on the so-far enigmatic role of cancer-associated mutations in genes encoding ribosomal proteins, with implications for our understanding of the tumor suppressive role of the RPL5/RPL11/5S rRNA complex in human malignancies.

Indexed as

MutationNeoplasmsProto-Oncogene Proteins c-mdm2Ribosomal ProteinsRibosomesTumor Suppressor Protein p53A549 CellsFemaleHumansMaleRNA, NeoplasmRNA, Ribosomal, 5SMDM2 protein, humanProto-Oncogene Proteins c-mdm2ribosomal protein L11ribosomal protein L5, humanRibosomal ProteinsRNA, NeoplasmRNA, Ribosomal, 5STP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID32108164
OpenAlexW3008397035

What OpenQuestion holds

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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.