Evidence map›Paper›PMID 19881544›Full record

ArticleOncogene2010

Notch3 cooperates with the EGFR pathway to modulate apoptosis through the induction of bim.

J Konishi, F Yi, X Chen, H Vo, D P Carbone, T P Dang

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.3field-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

57 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. NOTCH4Nature communications · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Cancer stem cells: a major culprit of intra-tumor heterogeneity.American journal of cancer research · 2021
    Review
  13. Article
  14. Targeting cancer stem cell pathways for cancer therapy.Signal transduction and targeted therapy · 2020
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. The Role ofThe oncologist · 2018
    Review
  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

6 authors at 1 institution in 1 country.

J KonishiDivision of Hematology and Medical Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.
F Yi
X Chen
H Vo
D P Carbone
T P Dang
Vanderbilt University Medical Center · US

Funding

Targeting Notch3 in Lung CancerR01CA115707 · NCI · VANDERBILT UNIVERSITY · PI DANG, THAO P. · 2007 to 2012
$1.3M
NCI NIH HHS 1R01 CA115707NCI NIH HHS R01 CA115707
6 · The paper itself

Abstract

Notch signaling is a highly conserved pathway important for normal embryonic development and cancer. We previously demonstrated a role for Notch3 in lung cancer pathogenesis. Notch3 inhibition resulted in tumor apoptosis and growth suppression. In vitro, these effects were enhanced when the epidermal growth factor receptor (EGFR) pathway was also inhibited, suggesting significant cross-talk between the two pathways. How Notch3 and epidermal growth factor receptor-mitogen-activated protein kinase (EGFR-MAPK) pathways cooperate in modulating apoptosis is not yet known. In this study, we provide evidence that Notch3 regulates Bim, a BH-3-only protein, via MAPK signaling. Furthermore, loss of Bim expression prevents tumor apoptosis induced by Notch3 inhibition. Using gamma-secretase inhibitor and erlotinib in a xenograft model, Bim induction and tumor inhibition were observed to be enhanced compared with either agent alone, consistent with our previous observation of significant synergism between Notch and EGFR-ras-MAPK signaling. Thus, our data support the hypothesis that Notch3 not only has a crucial role in lung cancer through regulating apoptosis, but also cooperates with the EGFR-MAPK pathway in modulating Bim.

Indexed as

ApoptosisMAP Kinase Signaling SystemAnimalsApoptosis Regulatory ProteinsBcl-2-Like Protein 11Cell Line, TumorErbB ReceptorsErlotinib HydrochlorideFemaleMembrane ProteinsMiceMice, NudeNeoplasmsProtein Kinase InhibitorsProto-Oncogene ProteinsQuinazolinesApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11ErbB ReceptorsErlotinib HydrochlorideMembrane ProteinsNOTCH3 protein, humanProtein Kinase InhibitorsProto-Oncogene ProteinsQuinazolinesReceptor, Notch3Receptors, NotchRNA, Small Interfering

Identifiers

PMID19881544
PMCPMC2813325
OpenAlexW2081828965

What OpenQuestion holds

Textmetadata
LicenceTDM
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.