EWI2 prevents EGFR from clustering and endocytosis to reduce tumor cell movement and proliferation.
And integrin
Clathrin-mediated endocytosis
Epithelial-to-mesenchymal transition
MAPK signaling
Membrane spatial heterogeneity
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
30 Jun 2022
30 Jun 2022
Historique:
received:
18
02
2022
accepted:
06
06
2022
revised:
27
05
2022
entrez:
30
6
2022
pubmed:
1
7
2022
medline:
6
7
2022
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 35773608
doi: 10.1007/s00018-022-04417-9
pii: 10.1007/s00018-022-04417-9
pmc: PMC10428948
mid: NIHMS1873543
doi:
Substances chimiques
Antigens, CD
0
IGSF8 protein, human
0
Integrins
0
Membrane Proteins
0
EGFR protein, human
EC 2.7.10.1
ErbB Receptors
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
389Subventions
Organisme : NCI NIH HHS
ID : P30 CA225520
Pays : United States
Organisme : Oklahoma Center for the Advancement of Science and Technology
ID : HR20-055
Organisme : Oklahoma Center for the Advancement of Science and Technology
ID : HR13-207
Informations de copyright
© 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.
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