Evidence map›Paper›PMID 28415746›Full record

ArticleOncotarget2017

Epigenetic up-regulation of ribosome biogenesis and more aggressive phenotype triggered by the lack of the histone demethylase JHDM1B in mammary epithelial cells.

Alice Galbiati, Marianna Penzo, Maria Giulia Bacalini, Carmine Onofrillo, Ania Naila Guerrieri, Paolo Garagnani, Claudio Franceschi, Davide Treré, Lorenzo Montanaro

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  16. Nucleolus and chromatin.Histochemistry and cell biology · 2018
    Review
  17. The critical role of histone lysine demethylase KDM2B in cancer.American journal of translational research · 2018
    Review
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 1 institution in 1 country.

Alice GalbiatiDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Marianna PenzoDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Maria Giulia BacaliniDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Carmine OnofrilloDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Ania Naila GuerrieriDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Paolo GaragnaniDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Claudio FranceschiDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Davide TreréDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
Lorenzo MontanaroDepartment of Experimental, Diagnostic, and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
University of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alterations of ribosome biogenesis and protein synthesis play a direct role in the development of tumors. The accessibility and transcription of ribosomal genes is controlled at several levels, with their epigenetic regulation being one of the most important. Here we explored the JmjC domain-containing histone demethylase 1B (JHDM1B) function in the epigenetic control of rDNA transcription. Since JHDM1B is a negative regulator of gene transcription, we focused on the effects induced by JHDM1B knock-down (KD). We studied the consequences of stable inducible JHDM1B silencing in cell lines derived from transformed and untransformed mammary epithelial cells. In these cellular models, prolonged JHDM1B downregulation triggered a surge of 45S pre-rRNA transcription and processing, associated with a re-modulation of the H3K36me2 levels at rDNA loci and with changes in DNA methylation of specific CpG sites in rDNA genes. We also found that after JHDM1B KD, cells showed a higher ribosome content: which were engaged in mRNA translation. JHDM1B KD and the consequent stimulation of ribosomes biogenesis conferred more aggressive features to the tested cellular models, which acquired a greater clonogenic, staminal and invasive potential. Taken together, these data indicate that the reduction of JHDM1B leads to a more aggressive cellular phenotype in mammary gland cells, by virtue of its negative regulatory activity on ribosome biogenesis.

Indexed as

Epigenesis, GeneticUp-RegulationAnimalsBreastBreast NeoplasmsCell LineCell Line, TumorEpithelial CellsF-Box ProteinsFemaleGene Expression Regulation, NeoplasticHistonesHumansJumonji Domain-Containing Histone DemethylasesMice, Inbred BALB CMice, NudeF-Box ProteinsHistonesJumonji Domain-Containing Histone DemethylasesKDM2A protein, humanRNA, RibosomalRNA, ribosomal, 45Scancer cellshistone modificationJHDM1BrDNAribosome biogenesis

Identifiers

PMID28415746
PMCPMC5514893
OpenAlexW2599068026

What OpenQuestion holds

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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.