Evidence map›Paper›PMID 11756662›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

CCAAT/enhancer binding protein-beta is a mediator of keratinocyte survival and skin tumorigenesis involving oncogenic Ras signaling.

Songyun Zhu, Kyungsil Yoon, Esta Sterneck, Peter F Johnson, Robert C Smart

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

106 citing papers in PubMed, 201 citations in OpenAlex.

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  10. RUNX1T1 function in cell fate.Stem cell research & therapy · 2022
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  17. Signal Transduction in Ribosome Biogenesis: A Recipe to Avoid Disaster.International journal of molecular sciences · 2019
    Review
  18. Article
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  20. Article

46 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Songyun ZhuCell Signaling and Cancer Group, Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695-7633, USA.
Kyungsil Yoon
Esta Sterneck
Peter F Johnson
Robert C Smart
North Carolina State University · USNational Cancer Institute · US

Funding

Role of C/EBPs in Squamous Differentiation and NeoplasiaR01CA046637 · NCI · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI SMART, ROBERT C · 1996 to 2011
$2.5M
DIACYLGLYCEROLS AS TUMOR PROMOTERSR29CA046637 · NCI · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI SMART, ROBERT C · 1990 to 1994
–
NCI NIH HHS CA46637NCI NIH HHS R01 CA046637
6 · The paper itself

Abstract

The basic leucine zipper transcription factor CCAAT/enhancer binding protein-beta (C/EBPbeta) is expressed in many cell types, including keratinocytes. C/EBPbeta activity can be increased by phosphorylation through pathways stimulated by oncogenic Ras, although the biological implications of Ras-C/EBPbeta signaling are not currently understood. We report here that C/EBPbeta-nullizygous mice are completely refractory to skin tumor development induced by a variety of carcinogens and carcinogenesis protocols, including 7,12-dimethylbenz[a]anthracene-initiation/12-O-tetradecanoylphorbol 13-acetate promotion, that produce tumors containing oncogenic Ras mutations. No significant differences in TPA-induced epidermal keratinocyte proliferation were observed in C/EBPbeta-null versus wild-type mice. However, apoptosis was significantly elevated (17-fold) in the epidermal keratinocytes of 7,12-dimethylbenz[a]anthracene-treated C/EBPbeta-null mice compared with wild-type mice. In v-Ha-ras transgenic mice, C/EBPbeta deficiency also led to greatly reduced skin tumor multiplicity and size, providing additional evidence for a tumorigenesis pathway linking Ras and C/EBPbeta. Oncogenic Ras potently stimulated C/EBPbeta to activate a C/EBP-responsive promoter-reporter in keratinocytes and mutating an ERK1/2 phosphorylation site (T188) in C/EBPbeta abolished this Ras effect. Finally, we observed that C/EBPbeta participates in oncogenic Ras-induced transformation of NIH 3T3 cells. These findings indicate that C/EBPbeta has a critical role in Ras-mediated tumorigenesis and cell survival and implicate C/EBPbeta as a target for tumor inhibition.

Indexed as

Signal Transduction3T3 Cells9,10-Dimethyl-1,2-benzanthraceneAnimalsApoptosisBlotting, WesternBromodeoxyuridineCarcinogensCCAAT-Enhancer-Binding Protein-betaCell DivisionCell SurvivalGenes, ReporterKeratinocytesMiceMice, Inbred BALB CMice, Transgenic9,10-Dimethyl-1,2-benzanthraceneBromodeoxyuridineCarcinogensCCAAT-Enhancer-Binding Protein-betaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesMutagensOncogene Protein p21(ras)Tetradecanoylphorbol Acetate

Identifiers

PMID11756662
PMCPMC117540
OpenAlexW2037742127

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.