Evidence map›Paper›PMID 21437251›Full record

ArticlePloS one2011

The Notch-2 gene is regulated by Wnt signaling in cultured colorectal cancer cells.

Jonas Ungerbäck, Nils Elander, John Grünberg, Mikael Sigvardsson, Peter Söderkvist

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Desmoid Tumors: Current Perspective and Treatment.Current treatment options in oncology · 2024
    Review
  8. Desmoid Tumors: A Comprehensive Review.Advances in therapy · 2023
    Review
  9. Review
  10. Signaling pathways and their potential therapeutic utility in esophageal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  11. Review
  12. Intestinal Wnt in the transition from physiology to oncology.World journal of clinical oncology · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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 1 institution in 1 country.

Jonas UngerbäckDivision of Cell Biology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköpings university, Linköping, Sweden. jonas.ungerback@liu.se
Nils Elander
John Grünberg
Mikael Sigvardsson
Peter Söderkvist
Linköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNotch and Wnt pathways are key regulators of intestinal homeostasis and alterations in these pathways may lead to the development of colorectal cancer (CRC). In CRC the Apc/β-catenin genes in the Wnt signaling pathway are frequently mutated and active Notch signaling contributes to tumorigenesis by keeping the epithelial cells in a proliferative state. These pathways are simultaneously active in proliferative adenoma cells and a crosstalk between them has previously been suggested in normal development as well as in cancer. PRINCIPAL

findingsIn this study, in silico analysis of putative promoters involved in transcriptional regulation of genes coding for proteins in the Notch signaling pathway revealed several putative LEF-1/TCF sites as potential targets for β-catenin and canonical Wnt signaling. Further results from competitive electrophoretic mobility-shift assay (EMSA) studies suggest binding of several putative sites in Notch pathway gene promoters to in vitro translated β-catenin/Lef-1. Wild type (wt)-Apc negatively regulates β-catenin. By induction of wt-Apc or β-catenin silencing in HT29 cells, we observed that several genes in the Notch pathway, including Notch-2, were downregulated. Finally, active Notch signaling was verified in the Apc(Min/+) mouse model where Hes-1 mRNA levels were found significantly upregulated in intestinal tumors compared to normal intestinal mucosa. Luciferase assays showed an increased activity for the core and proximal Notch-2 promoter upon co-transfection of HCT116 cells with high expression recombinant Tcf-4, Lef-1 or β-catenin.

conclusionsIn this paper, we identified Notch-2 as a novel target for β-catenin-dependent Wnt signaling. Furthermore our data supports the notion that additional genes in the Notch pathway might be transcriptionally regulated by Wnt signaling in colorectal cancer.

Indexed as

Gene Expression Regulation, NeoplasticAdenomaAnimalsBase SequenceBasic Helix-Loop-Helix Leucine Zipper Transcription Factorsbeta CateninBinding SitesColorectal NeoplasmsComputational BiologyHCT116 CellsHT29 CellsHumansLuciferasesLymphoid Enhancer-Binding Factor 1MiceMolecular Sequence DataBasic Helix-Loop-Helix Leucine Zipper Transcription Factorsbeta CateninLuciferasesLymphoid Enhancer-Binding Factor 1NOTCH2 protein, humanNotch2 protein, mouseReceptor, Notch2TCF4 protein, humanTranscription Factor 4Transcription FactorsWnt Proteins

Identifiers

PMID21437251
PMCPMC3060910
OpenAlexW2016542388

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.