Evidence map›Paper›PMID 29321661›Full record

ArticleOncogene2018

Differential recruitment of CD44 isoforms by ErbB ligands reveals an involvement of CD44 in breast cancer.

Iris Morath, Christian Jung, Romain Lévêque, Chen Linfeng, Robert-Alain Toillon, Arne Warth, Véronique Orian-Rousseau

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. 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
2.7field-weighted citation impact, top 10% 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, 41 citations in OpenAlex.

  1. Review
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  17. CDK5 Inhibition Abrogates TNBC Stem-Cell Property and Enhances Anti-PD-1 Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020
    Article
  18. Review
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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 5 institutions in 3 countries.

Iris MorathKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, Karlsruhe, Germany.
Christian JungKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, Karlsruhe, Germany.
Romain LévêqueUniv. Lille, Inserm, U908-CPAC-Cell Plasticity and Cancer, Lille, France.
Chen LinfengDana Farber Cancer Institute, Boston, MA, USA.
Robert-Alain ToillonUniv. Lille, Inserm, U908-CPAC-Cell Plasticity and Cancer, Lille, France.
Arne WarthInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Véronique Orian-RousseauKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, Karlsruhe, Germany. veronique.orian-rousseau@kit.edu.
Karlsruhe Institute of Technology · DEDana-Farber Cancer Institute · USInserm · FRUniversité de Lille · FRUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of the CD44 family of transmembrane glycoproteins control cell signaling pathways from numerous cell surface receptors, including receptor tyrosine kinases (RTKs). The decisive factor (ligand, RTKs or both) that controls the recruitment of specific CD44 isoforms is still unknown. We investigated this question by using the EGFR signaling pathway, in which one receptor can be activated by a broad range of ligands. By means of siRNA-mediated downregulation of CD44 expression and blocking experiments, we identified CD44v6 as a co-receptor for EGF- and ER-induced ErbB1 activation and for NRG1-induced ErbB3 and ErbB4 activation. In contrast, TGFα is independent of all CD44 isoforms, even though it addresses the same receptor pairs as EGF. Moreover, the heparin-sulfated CD44v3 isoform is required for HB-EGF-induced EGFR signaling. These data suggest that specific CD44 isoforms are recruited in a ligand-dependent manner as co-receptors in the EGFR signaling pathways and that the specificity is determined by the ligand and not by the receptors themselves. The in vivo relevance of this interplay between CD44 isoforms and EGFR ligands is underlined by the decreased metastatic spreading of mammary carcinomas in mice treated with a CD44v6-specific peptide. Most importantly, we found a clear correlation between the presence of CD44v6/ErbB1 complexes in breast cancer patients and lymph node metastases.

Indexed as

AnimalsBreast NeoplasmsCells, CulturedFemaleHT29 CellsHumansHyaluronan ReceptorsLigandsMCF-7 CellsMice, Inbred BALB CMice, Inbred C3HOncogene Proteins v-erbBProtein BindingProtein IsoformsSignal TransductionCD44 protein, humanHyaluronan ReceptorsLigandsOncogene Proteins v-erbBProtein Isoforms

Identifiers

PMID29321661
OpenAlexW2782584601

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.