Evidence map›Paper›PMID 25401168›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2015

Deregulation of the endogenous C/EBPβ LIP isoform predisposes to tumorigenesis.

Valérie Bégay, Jeske J Smink, Christoph Loddenkemper, Karin Zimmermann, Cornelia Rudolph, Marina Scheller, Doris Steinemann, Ulf Leser, Brigitte Schlegelberger, Harald Stein and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

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  12. EZH2 Supports Osteoclast Differentiation and Bone Resorption Via Epigenetic and Cytoplasmic Targets.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
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  19. EGFR and C/EBP-β oncogenic signaling is bidirectional in human glioma and varies with the C/EBP-β isoform.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  20. 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 4 institutions in 1 country.

Valérie BégayDepartment of Tumorigenesis and Cell Differentiation, Max Delbrueck Center for Molecular Medicine, Robert-Roessle-Str.10, 13125, Berlin, Germany.
Jeske J Smink
Christoph Loddenkemper
Karin Zimmermann
Cornelia Rudolph
Marina Scheller
Doris Steinemann
Ulf Leser
Brigitte Schlegelberger
Harald Stein
Achim Leutz
Max Delbrück Center · DEMedizinische Hochschule Hannover · DECharité - Universitätsmedizin Berlin · DEHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledTwo long and one truncated isoforms (termed LAP*, LAP, and LIP, respectively) of the transcription factor CCAAT enhancer binding protein beta (C/EBPβ) are expressed from a single intronless Cebpb gene by alternative translation initiation. Isoform expression is sensitive to mammalian target of rapamycin (mTOR)-mediated activation of the translation initiation machinery and relayed through an upstream open reading frame (uORF) on the C/EBPβ mRNA. The truncated C/EBPβ LIP, initiated by high mTOR activity, has been implied in neoplasia, but it was never shown whether endogenous C/EBPβ LIP may function as an oncogene. In this study, we examined spontaneous tumor formation in C/EBPβ knockin mice that constitutively express only the C/EBPβ LIP isoform from its own locus. Our data show that deregulated C/EBPβ LIP predisposes to oncogenesis in many tissues. Gene expression profiling suggests that C/EBPβ LIP supports a pro-tumorigenic microenvironment, resistance to apoptosis, and alteration of cytokine/chemokine expression. The results imply that enhanced translation reinitiation of C/EBPβ LIP promotes tumorigenesis. Accordingly, pharmacological restriction of mTOR function might be a therapeutic option in tumorigenesis that involves enhanced expression of the truncated C/EBPβ LIP isoform. KEY MESSAGE: Elevated C/EBPβ LIP promotes cancer in mice. C/EBPβ LIP is upregulated in B-NHL. Deregulated C/EBPβ LIP alters apoptosis and cytokine/chemokine networks. Deregulated C/EBPβ LIP may support a pro-tumorigenic microenvironment.

Indexed as

AnimalsCarcinogenesisCCAAT-Enhancer-Binding Protein-betaCells, CulturedCytokinesFibroblastsGene Expression ProfilingMice, KnockoutNeoplasmsProtein IsoformsCCAAT-Enhancer-Binding Protein-betaCytokinesProtein Isoforms

Identifiers

PMID25401168
OpenAlexW1967490566

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.