Lewis y Expressed in Oral Squamous Cell Carcinoma Attenuates Malignant Properties
Binding Sites
Cell Adhesion
Cell Line, Tumor
Cell Movement
Cell Shape
Epidermal Growth Factor
/ metabolism
ErbB Receptors
/ metabolism
Humans
Kinetics
Lewis Blood Group Antigens
/ metabolism
Mouth Neoplasms
/ metabolism
Neoplasm Invasiveness
Phosphorylation
Protein Binding
Signal Transduction
Squamous Cell Carcinoma of Head and Neck
/ metabolism
Lewis y
epidermal growth factor receptor
squamous cell carcinoma
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
10
02
2021
revised:
24
02
2021
accepted:
25
02
2021
entrez:
4
4
2021
pubmed:
5
4
2021
medline:
14
4
2021
Statut:
ppublish
Résumé
Lewis y is expressed in oral squamous cell carcinoma (OSCC) cells and tumors. Previously, we reported that Lewis y was not expressed in invasion areas, and attenuation of proliferation and invasion in OSCC cells was caused by over-expression of Lewis y. However, the roles of Lewis y in the attenuation of malignant properties have not been clarified. In this study, we investigated the roles of Lewis y in OSCC. The levels of Lewis y on EGFR and the phosphorylation levels of EGFR in OSCC cells were analyzed by immunoprecipitation and western blot. EGFR cross-linking and binding kinetics of EGF were performed. Upon EGF stimulation, phosphorylation and dimer formation of EGFR were more prominent in Lewis y- cells. EGF binding kinetics showed reduced binding sites in Lewis y+ cells. Lewis y reduced EGF binding to EGFR, leading to suppression of malignant properties through suppression of EGF signaling.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
Lewis y is expressed in oral squamous cell carcinoma (OSCC) cells and tumors. Previously, we reported that Lewis y was not expressed in invasion areas, and attenuation of proliferation and invasion in OSCC cells was caused by over-expression of Lewis y. However, the roles of Lewis y in the attenuation of malignant properties have not been clarified. In this study, we investigated the roles of Lewis y in OSCC.
MATERIALS AND METHODS
METHODS
The levels of Lewis y on EGFR and the phosphorylation levels of EGFR in OSCC cells were analyzed by immunoprecipitation and western blot. EGFR cross-linking and binding kinetics of EGF were performed.
RESULTS
RESULTS
Upon EGF stimulation, phosphorylation and dimer formation of EGFR were more prominent in Lewis y- cells. EGF binding kinetics showed reduced binding sites in Lewis y+ cells.
CONCLUSION
CONCLUSIONS
Lewis y reduced EGF binding to EGFR, leading to suppression of malignant properties through suppression of EGF signaling.
Identifiants
pubmed: 33813387
pii: 41/4/1821
doi: 10.21873/anticanres.14948
doi:
Substances chimiques
Lewis Blood Group Antigens
0
Lewis Y antigen
0
Epidermal Growth Factor
62229-50-9
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
1821-1830Informations de copyright
Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.