Evidence map›Paper›PMID 12592391›Full record

ArticleOncogene2003

IRF-1 reverts the transformed phenotype of oncogenically transformed cells in vitro and in vivo.

Andrea Kröger, Andreas Dallügge, Sabine Kirchhoff, Hansjörg Hauser

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 59 citations in OpenAlex.

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  15. Roles of IKK-beta, IRF1, and p65 in the activation of chemokine genes by interferon-gamma.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2009
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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

4 authors at 1 institution in 1 country.

Andrea KrögerDepartment of Gene Regulation and Differentiation, GBF - German Research Center for Biotechnology, Mascheroder Weg 1, D 38124 Braunschweig, Germany.
Andreas Dallügge
Sabine Kirchhoff
Hansjörg Hauser
German Center for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of the transcriptional activator and tumor suppressor IRF-1 induces multiple effects that counteract the growth of tumor cells in vitro and in vivo. These include the inhibition of cell proliferation, the secretion of interferon-beta (IFN-beta), the induction of apoptosis specifically in certain cell types and the induction of a strong T-cell response. Here, we show that apart from its immune-activating properties, IRF-1 expression leads to a reversion of the tumorigenic phenotype of NIH3T3 cells transformed by different oncogenes. This was analysed in detail in a cell line in which the expression of c-Ha-ras and c-myc is under the control of a doxycycline-regulated promoter allowing to switch between the normal and oncogenic cell status. In the same cells, a beta-estradiol activatable IRF-1 fusion protein is expressed. After IRF-1 activation the oncogene-mediated acceleration of the cell cycle is reverted. Further, a complete IRF-1-mediated reversion of the oncogenic phenotype is observed in soft-agar growth assays. IRF-1 activation induces IFN-beta secretion; however, the observed effects are not mediated by IFN-beta. Inhibition of tumor growth is observed in nude mice as long as IRF-1 is active, indicating that neither B- nor T-cells must become activated for tumor growth suppression.

Indexed as

Genes, erbB-1Genes, erbB-2Genes, mycGenes, ras3T3 CellsAnimalsCell CycleCell DivisionCell Transformation, NeoplasticDNA-Binding ProteinsDoxycyclineEstradiolHumansInterferon-betaInterferon Regulatory Factor-1MaleDNA-Binding ProteinsDoxycyclineEstradiolInterferon-betaInterferon Regulatory Factor-1IRF1 protein, humanIrf1 protein, mousePhosphoproteinsReceptors, EstrogenRecombinant Fusion Proteins

Identifiers

PMID12592391
OpenAlexW2015141576

What OpenQuestion holds

Textmetadata
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.