Evidence map›Paper›PMID 33255756›Full record

ArticleCancers2020

DKC1 Overexpression Induces a More Aggressive Cellular Behavior and Increases Intrinsic Ribosomal Activity in Immortalized Mammary Gland Cells.

Ania Naila Guerrieri, Federico Zacchini, Carmine Onofrillo, Sara Di Viggiano, Marianna Penzo, Alessio Ansuini, Ilaria Gandin, Yuko Nobe, Masato Taoka, Toshiaki Isobe and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

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  10. Small nucleolar RNAs: the hidden precursors of cancer ribosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  11. Article
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  16. RNA modifications in cancer.British journal of cancer · 2023
    Review
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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

12 authors at 4 institutions in 2 countries.

Ania Naila GuerrieriDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.ORCID 0000-0002-2163-6476
Federico ZacchiniDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.ORCID 0000-0002-6038-1779
Carmine OnofrilloDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.ORCID 0000-0002-1076-6419
Sara Di ViggianoDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.
Marianna PenzoDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.ORCID 0000-0002-1738-9767
Alessio AnsuiniResearch Unit, AREA Science Park, Padriciano, 99, 34149 Trieste, Italy.
Ilaria GandinResearch Unit, AREA Science Park, Padriciano, 99, 34149 Trieste, Italy.
Yuko NobeDepartment of Chemistry, Graduate School of Science and Engineering, Tokyo Metropolitan University, Minami-osawa 1-1, Hachioji-shi, Tokyo 192-0397, Japan.
Masato TaokaDepartment of Chemistry, Graduate School of Science and Engineering, Tokyo Metropolitan University, Minami-osawa 1-1, Hachioji-shi, Tokyo 192-0397, Japan.ORCID 0000-0001-5554-4951
Toshiaki IsobeDepartment of Chemistry, Graduate School of Science and Engineering, Tokyo Metropolitan University, Minami-osawa 1-1, Hachioji-shi, Tokyo 192-0397, Japan.
Davide TreréDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.ORCID 0000-0003-1127-1052
Lorenzo MontanaroDepartment of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy.ORCID 0000-0001-9776-9518
University of Bologna · ITTokyo Metropolitan University · JPAREA Science Park · ITAzienda USL di Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dyskerin is a nucleolar protein involved in the small nucleolar RNA (snoRNA)-guided pseudouridylation of specific uridines on ribosomal RNA (rRNA), and in the stabilization of the telomerase RNA component (hTR). Loss of function mutations in DKC1 causes X-linked dyskeratosis congenita, which is characterized by a failure of proliferating tissues and increased susceptibility to cancer. However, several tumors show dyskerin overexpression. We observed that patients with primary breast cancers with high dyskerin levels are more frequently characterized by shorter survival rates and positive lymph node status than those with tumors with a lower dyskerin expression. To functionally characterize the effects of high dyskerin expression, we generated stably overexpressing DKC1 models finding that increased dyskerin levels conferred a more aggressive cellular phenotype in untransformed immortalized MCF10A cells. Contextually, DKC1 overexpression led to an upregulation of some snoRNAs, including SNORA67 and a significantly increased U1445 modification on 18S rRNA, the known target of SNORA67. Lastly, we found that dyskerin overexpression strongly enhanced the synthetic activity of ribosomes increasing translational efficiency in MCF10A. Altogether, our results indicate that dyskerin may sustain the neoplastic phenotype from an early stage in breast cancer endowing ribosomes with an augmented translation efficiency.

Indexed as

breast cancerDKC1dyskerinprognosispseudouridylationrRNAsnoRNA

Identifiers

PMID33255756
PMCPMC7760958
OpenAlexW3108218931

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.