EGFR trafficking: effect of dimerization, dynamics, and mutation

Spontaneous dimerization of EGF receptors (EGFR) and dysregulation of EGFR signaling has been associated with the development of different cancers. Under normal physiological conditions and to maintain homeostatic cell growth, once EGFR signaling occurs, it needs to be attenuated. Activated EGFRs ar...

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Published inFrontiers in oncology Vol. 13; p. 1258371
Main Authors Schultz, Destiny F, Billadeau, Daniel D, Jois, Seetharama D
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 11.09.2023
Subjects
cancer
clathrin-mediated endocytosis
dimerization
EGFR trafficking
lysosome
Oncology
dimerization
cancer
EGFR trafficking
lysosome
clathrin-mediated endocytosis
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Summary:Spontaneous dimerization of EGF receptors (EGFR) and dysregulation of EGFR signaling has been associated with the development of different cancers. Under normal physiological conditions and to maintain homeostatic cell growth, once EGFR signaling occurs, it needs to be attenuated. Activated EGFRs are rapidly internalized, sorted through early endosomes, and ultimately degraded in lysosomes by a process generally known as receptor down-regulation. Through alterations to EGFR trafficking, tumors develop resistance to current treatment strategies, thus highlighting the necessity for combination treatment strategies that target EGFR trafficking. This review covers EGFR structure, trafficking, and altered surface expression of EGFR receptors in cancer, with a focus on how therapy targeting EGFR trafficking may aid tyrosine kinase inhibitor treatment of cancer.
Bibliography:ObjectType-Article-2
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Reviewed by: Yongkun Wei, University of Texas MD Anderson Cancer Center, United States; Evin Iscan, Dokuz Eylül University, Türkiye; Shravan Girada, University of California, San Diego, United States; Paras Gaur, The University of Iowa, United States
Edited by: Anurag Kumar Singh, Martin Luther University of Halle-Wittenberg, Germany
ISSN:2234-943X
2234-943X
DOI:10.3389/fonc.2023.1258371