Evidence map›Paper›PMID 24528514›Full record

ArticleJournal of experimental & clinical cancer research : CR2014

Poly (ADP-ribose) polymerase 3 (PARP3), a potential repressor of telomerase activity.

Tamara Fernández-Marcelo, Cristina Frías, Irene Pascua, Carmen de Juan, Jacqueline Head, Ana Gómez, Florentino Hernando, Jose-Ramon Jarabo, Eduardo Díaz-Rubio, Antonio-Jose Torres and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  6. DNA damage and tissue repair: What we can learn from planaria.Seminars in cell & developmental biology · 2019
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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

13 authors at 2 institutions in 2 countries.

Tamara Fernández-Marcelo
Cristina Frías
Irene Pascua
Carmen de Juan
Jacqueline Head
Ana Gómez
Florentino Hernando
Jose-Ramon Jarabo
Eduardo Díaz-Rubio
Antonio-Jose Torres
Michèle Rouleau
Manuel Benito
Pilar IniestaDepartamento de Bioquímica y Biología Molecular II, Facultad de Farmacia, Universidad Complutense y Servicios de, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid 28040, Spain. insepi@ucm.es.
Instituto de Investigación Sanitaria del Hospital Clínico San Carlos · ESUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundConsidering previous result in Non-Small Cell Lung Cancer (NSCLC), we investigated in human cancer cells the role of PARP3 in the regulation of telomerase activity.

methodsWe selected A549 (lung adenocarcinoma cell line) and Saos-2 (osteosarcoma cell line), with high and low telomerase activity levels, respectively. The first one was transfected using a plasmid construction containing a PARP3 sequence, whereas the Saos-2 cells were submitted to shRNA transfection to get PARP3 depletion. PARP3 expression on both cell systems was evaluated by real-time quantitative PCR and PARP3 protein levels, by Western-blot. Telomerase activity was determined by TRAP assay.

resultsIn A549 cells, after PARP3 transient transfection, data obtained indicated that twenty-four hours after transfection, up to 100-fold increased gene expression levels were found in the transfected cells with pcDNA/GW-53/PARP3 in comparison to transfected cells with the empty vector. Moreover, 48 hours post-transfection, telomerase activity decreased around 33%, and around 27%, 96 hours post-transfection. Telomerase activity average ratio was 0.67 ± 0.05, and 0.73 ± 0.06, respectively, with significant differences. In Saos-2 cells, after shRNA-mediated PARP3 silencing, a 2.3-fold increase in telomerase activity was detected in relation to the control.

conclusionOur data indicated that, at least in some cancer cells, repression of PARP3 could be responsible for an increased telomerase activity, this fact contributing to telomere maintenance and, therefore, avoiding genome instability.

Indexed as

Cell Cycle ProteinsCell Line, TumorGene Expression Regulation, EnzymologicGene Knockdown TechniquesHumansPoly(ADP-ribose) PolymerasesRNA, MessengerRNA, Small InterferingTelomeraseCell Cycle ProteinsPARP3 protein, humanPoly(ADP-ribose) PolymerasesRNA, MessengerRNA, Small InterferingTelomerase

Identifiers

PMID24528514
PMCPMC3937032
OpenAlexW2136163553

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.