Evidence map›Paper›PMID 35773608›Full record

ArticleCellular and molecular life sciences : CMLS2022

EWI2 prevents EGFR from clustering and endocytosis to reduce tumor cell movement and proliferation.

Chenying Fu, Jie Wang, Sandeep Pallikkuth, Yingjun Ding, Junxiong Chen, Jonathan D Wren, Yuchao Yang, Kwong-Kwok Wong, Hiroyasu Kameyama, Muralidharan Jayaraman and 4 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

14 authors at 4 institutions in 1 country.

Chenying Fu *University of Oklahoma Health Sciences Center, Oklahoma City, USA.
Jie Wang *University of Oklahoma Health Sciences Center, Oklahoma City, USA.
Sandeep PallikkuthUniversity of New Mexico, Albuquerque, USA.
Yingjun DingUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Junxiong ChenUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Jonathan D WrenOklahoma Medical Research Foundation, Oklahoma City, USA.
Yuchao YangUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Kwong-Kwok WongUniversity of Texas MD Anderson Cancer Center, Houston, USA.
Hiroyasu KameyamaUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Muralidharan JayaramanUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Anupama MunshiUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Takemi TanakaUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA.
Keith A LidkeUniversity of New Mexico, Albuquerque, USA.
Xin A ZhangUniversity of Oklahoma Health Sciences Center, Oklahoma City, USA. xin-zhang-1@ouhsc.edu.ORCID http://orcid.org/0000-0001-5074-3847
University of Oklahoma Health Sciences Center · USUniversity of New Mexico · USOklahoma Medical Research Foundation · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tissue Pathology Shared ResourceP30CA225520 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Wade Williams · 2018 to 2026
$27.1M
NCI NIH HHS P30 CA225520Oklahoma Center for the Advancement of Science and Technology HR13-207Oklahoma Center for the Advancement of Science and Technology HR20-055
6 · The paper itself

Abstract

EWI2 is a transmembrane immunoglobulin superfamily (IgSF) protein that physically associates with tetraspanins and integrins. It inhibits cancer cells by influencing the interactions among membrane molecules including the tetraspanins and integrins. The present study revealed that, upon EWI2 silencing or ablation, the elevated movement and proliferation of cancer cells in vitro and increased cancer metastatic potential and malignancy in vivo are associated with (i) increases in clustering, endocytosis, and then activation of EGFR and (ii) enhancement of Erk MAP kinase signaling. These changes in signaling make cancer cells (i) undergo partial epithelial-to-mesenchymal (EMT) for more tumor progression and (ii) proliferate faster for better tumor formation. Inhibition of EGFR or Erk kinase can abrogate the cancer cell phenotypes resulting from EWI2 removal. Thus, to inhibit cancer cells, EWI2 prevents EGFR from clustering and endocytosis to restrain its activation and signaling.

Indexed as

Antigens, CDEndocytosisErbB ReceptorsMembrane ProteinsNeoplasmsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansIntegrinsAntigens, CDEGFR protein, humanErbB ReceptorsIGSF8 protein, humanIntegrinsMembrane ProteinsAnd integrinClathrin-mediated endocytosisEpithelial-to-mesenchymal transitionMAPK signalingMembrane spatial heterogeneity

Identifiers

PMID35773608
PMCPMC10428948
OpenAlexW4283714733

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.