Evidence map›Paper›PMID 27374104›Full record

ArticleOncotarget2016

RPL27A is a target of miR-595 and may contribute to the myelodysplastic phenotype through ribosomal dysgenesis.

Heba A Alkhatabi, Donal P McLornan, Austin G Kulasekararaj, Farooq Malik, Thomas Seidl, David Darling, Joop Gaken, Ghulam J Mufti

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  5. Ribosome biogenesis in disease: new players and therapeutic targets.Signal transduction and targeted therapy · 2023
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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

8 authors at 3 institutions in 2 countries.

Heba A AlkhatabiDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
Donal P McLornanDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
Austin G KulasekararajDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
Farooq MalikDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
Thomas SeidlDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
David DarlingDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
Joop GakenDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
Ghulam J MuftiDepartment of Haematological Medicine, King's College London School of Medicine, London, UK.
King's College School · GBKing's College London · GBKing's College Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the functional consequences following deletion of a microRNA (miR) termed miR-595 which resides on chromosome 7q and is localised within one of the commonly deleted regions identified for Myelodysplasia (MDS) with monosomy 7 (-7)/isolated loss of 7q (7q-). We identified several targets for miR-595, including a large ribosomal subunit protein RPL27A. RPL27A downregulation induced p53 activation, apoptosis and inhibited proliferation. Moreover, p53-independent effects were additionally identified secondary to a reduction in the ribosome subunit 60s. We confirmed that RPL27A plays a pivotal role in the maintenance of nucleolar integrity and ribosomal synthesis/maturation. Of note, RPL27A overexpression, despite showing no significant effects on p53 mRNA levels, did in fact enhance cellular proliferation. In normal CD34+ cells, RPL27A knockdown preferentially blocked erythroid proliferation and differentiation. Lastly, we show that miR-595 expression appears significantly downregulated in the majority of primary samples derived from MDS patients with (-7)/(7q-), in association with RPL27A upregulation. This significant downregulation of miR-595 is also apparent when higher risk MDS cases are compared to lower risk cases. The potential clinical importance of these findings requires further validation.

Indexed as

Cell ProliferationCohort StudiesGene Knockdown TechniquesHCT116 CellsHeLa CellsHep G2 CellsHumansK562 CellsMCF-7 CellsMicroRNAsMyelodysplastic SyndromesPhenotypeRibosomal ProteinsRibosomesTransfectionU937 CellsmicroRNA595 microRNA, humanMicroRNAsRibosomal ProteinsRPL27A protein, humanchromosomehaemopoiesismicroRNAmyelodysplasiaribosome

Identifiers

PMID27374104
PMCPMC5216985
OpenAlexW2471225454

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.