Evidence map›Paper›PMID 38509231›Full record

ArticleOncogene2024

E-cadherin interacts with EGFR resulting in hyper-activation of ERK in multiple models of breast cancer.

Gabriella C Russo, Ashleigh J Crawford, David Clark, Julie Cui, Ryan Carney, Michelle N Karl, Boyang Su, Bartholomew Starich, Tung-Shing Lih, Pratik Kamat and 8 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
8.2field-weighted citation impact, top 2% 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, 29 citations in OpenAlex.

  1. Article
  2. E-cadherin expression promotes tumor growth via KLRG1-dependent pathways.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 3 institutions in 2 countries.

Gabriella C RussoDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Ashleigh J CrawfordDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
David ClarkDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Julie CuiDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Ryan CarneyDepartment of Biophysics, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Michelle N KarlDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Boyang SuDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
Bartholomew StarichDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Tung-Shing LihDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Pratik KamatDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Qiming ZhangDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Praful R NairDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Pei-Hsun WuDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.ORCID 0000-0002-7371-2960
Meng-Horng LeeDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA.
Hon S LeongDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
Hui ZhangDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Vito W RebeccaDepartment of Biochemistry and Molecular Biology, Johns Hopkins University School of Public Health, Baltimore, MD, 21231, USA.
Denis WirtzDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, 3400 N Charles St, Baltimore, MD, 21218, USA. wirtz@jhu.edu.ORCID 0000-0001-6147-3045
Johns Hopkins University · USSunnybrook Health Science Centre · CAUniversity of Toronto · CA

Funding

TRANS NETWORK PROJECTSU54CA143868 · NCI · JOHNS HOPKINS UNIVERSITY · PI WIRTZ, DENIS · 2009 to 2013
$13.7M
Tech Core 2U54CA268083 · NCI · JOHNS HOPKINS UNIVERSITY · PI Denis Wirtz, Laura DeLong Wood · 2022 to 2026
$10.2M
Validation of Nuclear Morphology as a Biomarker of Aging and Aging-Related PhenotypesU01AG060903 · NIA · JOHNS HOPKINS UNIVERSITY · PI WIRTZ, DENIS · 2018 to 2022
$3.1M
Three-dimensional maps of senescence in the human pancreasUG3CA275681 · NCI · JOHNS HOPKINS UNIVERSITY · PI WU, PEI-HSUN · 2022 to 2023
$1.1M
NCI NIH HHS U54 CA143868NCI NIH HHS UG3 CA275681U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) U01AG060903U.S. Department of Health & Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics) U54CA268083U.S. Department of Health & Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics) UG3CA275681
6 · The paper itself

Abstract

The loss of intercellular adhesion molecule E-cadherin is a hallmark of the epithelial-mesenchymal transition (EMT), during which tumor cells transition into an invasive phenotype. Accordingly, E-cadherin has long been considered a tumor suppressor gene; however, E-cadherin expression is paradoxically correlated with breast cancer survival rates. Using novel multi-compartment organoids and multiple in vivo models, we show that E-cadherin promotes a hyper-proliferative phenotype in breast cancer cells via interaction with the transmembrane receptor EGFR. The E-cad and EGFR interaction results in activation of the MEK/ERK signaling pathway, leading to a significant increase in proliferation via activation of transcription factors, including c-Fos. Pharmacological inhibition of MEK activity in E-cadherin positive breast cancer significantly decreases both tumor growth and macro-metastasis in vivo. This work provides evidence for a novel role of E-cadherin in breast tumor progression and identifies a new target to treat hyper-proliferative E-cadherin-positive breast tumors, thus providing the foundation to utilize E-cadherin as a biomarker for specific therapeutic success.

Indexed as

Antigens, CDBreast NeoplasmsCadherinsCell ProliferationErbB ReceptorsAnimalsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHumansMAP Kinase Signaling SystemMiceAntigens, CDCadherinsCDH1 protein, humanEGFR protein, humanErbB Receptors

Identifiers

PMID38509231
OpenAlexW4393010937

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.