Evidence map›Paper›PMID 9990071›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Target genes of beta-catenin-T cell-factor/lymphoid-enhancer-factor signaling in human colorectal carcinomas.

B Mann, M Gelos, A Siedow, M L Hanski, A Gratchev, M Ilyas, W F Bodmer, M P Moyer, E O Riecken, H J Buhr and 1 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 294 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
294citing papers in PubMed, 2 pooled it
19.5field-weighted citation impact, top 1% 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

294 citing papers in PubMed, 2 syntheses or guidelines pooled it, 808 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Review
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234 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

11 authors at 2 institutions in 2 countries.

B MannDepartment of Surgery, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, 12200 Berlin, Germany. mann@ukbf.fu-berlin.de
M Gelos
A Siedow
M L Hanski
A Gratchev
M Ilyas
W F Bodmer
M P Moyer
E O Riecken
H J Buhr
C Hanski
Freie Universität Berlin · DECancer Genetics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the adenomatous polyposis coli or beta-catenin gene lead to cytosolic accumulation of beta-catenin and, subsequently, to increased transcriptional activity of the beta-catenin-T cell-factor/lymphoid-enhancer-factor complex. This process seems to play an essential role in the development of most colorectal carcinomas. To identify genes activated by beta-catenin overexpression, we used colorectal cell lines for transfection with the beta-catenin gene and searched for genes differentially expressed in the transfectants. There are four genes affected by beta-catenin overexpression; three overexpressed genes code for two components of the AP-1 transcription complex, c-jun and fra-1, and for the urokinase-type plasminogen activator receptor (uPAR), whose transcription is activated by AP-1. The direct interaction of the beta-catenin-T cell-factor/lymphoid-enhancer-factor complex with the promoter region of c-jun and fra-1 was shown in a gel shift assay. The concomitant increase in beta-catenin expression and the amount of uPAR was confirmed in primary colon carcinomas and their liver metastases at both the mRNA and the protein levels. High expression of beta-catenin in transfectants, as well as in additionally analyzed colorectal cell lines, was associated with decreased expression of ZO-1, which is involved in epithelial polarization. Thus, accumulation of beta-catenin indirectly affects the expression of uPAR in vitro and in vivo. Together with the other alterations, beta-catenin accumulation may contribute to the development and progression of colon carcinoma both by dedifferentiation and through proteolytic activity.

Indexed as

Genes, APCSignal TransductionTrans-ActivatorsAdenocarcinomabeta CateninCadherinsCell LineCell PolarityColonColonic NeoplasmsColorectal NeoplasmsCytoskeletal ProteinsFos-Related Antigen 1Gene Expression Regulation, NeoplasticGenes, junHumansbeta CateninCadherinsCTNNB1 protein, humanCytoskeletal ProteinsFos-Related Antigen 1Membrane ProteinsNF-kappa BPhosphoproteinsPLAUR protein, humanProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junReceptors, Cell SurfaceReceptors, Urokinase Plasminogen ActivatorRecombinant ProteinsTJP1 protein, humanTrans-ActivatorsTranscription Factor AP-1Urokinase-Type Plasminogen ActivatorZonula Occludens-1 Protein

Identifiers

PMID9990071
PMCPMC15532
OpenAlexW2014995450

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.