Evidence map›Paper›PMID 19212434›Full record

ArticlePloS one2009

Dual role of Sp3 transcription factor as an inducer of apoptosis and a marker of tumour aggressiveness.

Khadija Essafi-Benkhadir, Sébastien Grosso, Alexandre Puissant, Guillaume Robert, Makram Essafi, Marcel Deckert, Emmanuel Chamorey, Olivier Dassonville, Gérard Milano, Patrick Auberger and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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  6. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
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  20. Glutamine protects against apoptosis via downregulation of Sp3 in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2010
    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

11 authors at 6 institutions in 2 countries.

Khadija Essafi-BenkhadirUniversity of Nice-Sophia Antipolis, Institute of Developmental Biology and Cancer Research UMR CNRS 6543, Centre Antoine Lacassagne, Nice, France.
Sébastien Grosso
Alexandre Puissant
Guillaume Robert
Makram Essafi
Marcel Deckert
Emmanuel Chamorey
Olivier Dassonville
Gérard Milano
Patrick Auberger
Gilles Pagès
Centre Antoine Lacassagne · FRInserm · FRLa Ligue Contre le Cancer · FRUniversité Côte d'Azur · FRCentre National de la Recherche Scientifique · FRMRC Biostatistics Unit · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe ambiguous role of transcription factor Sp3 for tumour progression is still debated since it was described as a transcriptional repressor or activator. Here we tried to decipher the molecular mechanisms implicated in Sp3 accumulation observed in aggressive tumours. METHODOLOGY: We generated normal and tumour cell lines conditionally expressing Sp3. Cell growth was analyzed in vitro and after inoculation in nude mice. Apoptosis was assessed by pan- caspase activity assays, by counting fragmented nuclei and by determination of caspase 9 cleavage. Gene expression was determined by quantitative PCR. Cleavage by different caspases was performed after in vitro translation of the Sp3 cDNA in the presence of [S(35)] labelled methionine. Different tumour cell lines and head and neck tumour samples were tested for the presence of Sp3 by western blots. Correlation between Sp3 expression and overall survival has been statistically determined. PRINCIPAL

findingsConditional over-expression of Sp3 induces apoptosis and modifies expression of genes implicated in the regulation of cell cycle and pro and anti apoptotic genes. Sp3 over-expression strongly reduces the development of tumours in nude mice confirming its pro-apoptotic potential in vivo. However, cells can survive to apoptosis through selective Sp3 cleavage by caspase. Sp3 induction in established tumours resulted in transient regression then progression. Progression coincides with re-accumulation of the full length form of Sp3. Sp3 is over-expressed in tumour cell lines of different origins. The presence of high levels of the full-length form of Sp3 indicates a poor prognosis for overall survival of patients with head and neck tumours.

conclusionsFull length Sp3 accumulation highlights bypass of tumour cell apoptotic capacities and is indicative of head and neck tumours aggressiveness.

Indexed as

AnimalsApoptosisCaspasesCell Line, TumorGene ExpressionGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansMiceMice, NudeNeoplasmsNeoplasm TransplantationPrognosisSp3 Transcription FactorSurvival RateCaspasesSp3 Transcription Factor

Identifiers

PMID19212434
PMCPMC2636865
OpenAlexW2007538671

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.