Evidence map›Paper›PMID 18952597›Full record

ArticleCarcinogenesis2008

c-Jun N-terminal kinase 1 interacts with and negatively regulates Wnt/beta-catenin signaling through GSK3beta pathway.

Dong Hu, Wenfeng Fang, Anjia Han, Lindsay Gallagher, Roger J Davis, Bin Xiong, Wancai Yang

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  7. Expansion of cancer stem cell pool initiates lung cancer recurrence before angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  8. Stromal expression of JNK1 and VDR is associated with the prognosis of esophageal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    Article
  9. Article
  10. Tetraspanin-2 promotes glucotoxic apoptosis by regulating the JNK/β-catenin signaling pathway in human pancreatic β cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
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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

7 authors at 4 institutions in 2 countries.

Dong HuDepartment of Pathology, University of Illinois at Chicago, Chicago, IL 60612, USA.
Wenfeng Fang
Anjia Han
Lindsay Gallagher
Roger J Davis
Bin Xiong
Wancai Yang
University of Illinois Chicago · USWuhan University · CNHoward Hughes Medical Institute · USSun Yat-sen University · CN

Funding

Intestinal Cancer Chemoprevention: Molecular MechanismsR01CA112081 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI YANG, WANCAI · 2005 to 2009
$1.1M
NCI NIH HHS R01 CA112081
6 · The paper itself

Abstract

Increasing evidence shows that there is an interaction between mitogen-activated protein kinase and Wnt signaling and that their interaction plays important roles in a variety of cellular processes. However, how the two signaling interacts is not clear. In this study, we found that beta-catenin expression was strikingly increased in the intestinal normal mucosa and tumors of c-Jun N-terminal kinase (JNK) 1-deficient mice by immunohistochemical staining and that both beta-catenin expression and transcriptional activity were significantly upregulated in JNK1-deficient mouse embryonic fibroblasts. However, active JNK1 significantly inhibited beta-catenin expression and suppressed beta-catenin-mediated transcriptional activity by enhancing glycogen synthase kinase 3beta (GSK3beta) activity. But beta-catenin inhibition was significantly reduced by GSK3beta RNA interference or GSK3beta inhibitor lithium chloride and proteasome inhibitor MG132. Further, mutant beta-catenin at the phosphorylation sites of Ser33 and Ser37 by GSK3beta was resistant to activated JNK1-induced beta-catenin degradation. Moreover, the physical interaction between JNK1 and beta-catenin was detected by immunoprecipitation, and their colocalization was seen in cellular nuclei and cytoplasm. Taken together, our data provide direct evidence that JNK1 interacts with and negatively regulates beta-catenin signaling through GSK3beta pathway and that the beta-catenin alteration is probably responsible for the intestinal tumor formation in JNK1-deficient mice.

Indexed as

Animalsbeta CateninBlotting, WesternCell Line, TumorCell Transformation, NeoplasticFluorescent Antibody TechniqueGlycogen Synthase Kinase 3HumansImmunohistochemistryIntestinal MucosaIntestinal NeoplasmsMiceMice, Mutant StrainsMitogen-Activated Protein Kinase 8Signal TransductionTransfectionbeta CateninGlycogen Synthase Kinase 3Mitogen-Activated Protein Kinase 8Wnt Proteins

Identifiers

PMID18952597
PMCPMC2639245
OpenAlexW2116465977

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.