FGF/FGFR signaling in adrenocortical development and tumorigenesis: novel potential therapeutic targets in adrenocortical carcinoma.
Adrenocortical development
Adrenocortical tumors
FGF-pathway
FGFR
FGFR-inhibitors
Journal
Endocrine
ISSN: 1559-0100
Titre abrégé: Endocrine
Pays: United States
ID NLM: 9434444
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
received:
30
03
2022
accepted:
08
05
2022
pubmed:
19
5
2022
medline:
20
8
2022
entrez:
18
5
2022
Statut:
ppublish
Résumé
FGF/FGFR signaling regulates embryogenesis, angiogenesis, tissue homeostasis and wound repair by modulating proliferation, differentiation, survival, migration and metabolism of target cells. Understandably, compelling evidence for deregulated FGF signaling in the development and progression of different types of tumors continue to emerge and FGFR inhibitors arise as potential targeted therapeutic agents, particularly in tumors harboring aberrant FGFR signaling. There is first evidence of a dual role of the FGF/FGFR system in both organogenesis and tumorigenesis, of which this review aims to provide an overview. FGF-1 and FGF-2 are expressed in the adrenal cortex and are the most powerful mitogens for adrenocortical cells. Physiologically, they are involved in development and maintenance of the adrenal gland and bind to a family of four tyrosine kinase receptors, among which FGFR1 and FGFR4 are the most strongly expressed in the adrenal cortex. The repeatedly proven overexpression of these two FGFRs also in adrenocortical cancer is thus likely a sign of their participation in proliferation and vascularization, though the exact downstream mechanisms are not yet elucidated. Thus, FGFRs potentially offer novel therapeutic targets also for adrenocortical carcinoma, a type of cancer resistant to conventional antimitotic agents.
Identifiants
pubmed: 35583844
doi: 10.1007/s12020-022-03074-z
pii: 10.1007/s12020-022-03074-z
pmc: PMC9385797
doi:
Substances chimiques
Receptors, Fibroblast Growth Factor
0
Fibroblast Growth Factors
62031-54-3
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
411-418Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2022. The Author(s).
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