Intracellular FGF1 protects cells from apoptosis through direct interaction with p53.
Anti-apoptotic activity
Apoptosis
Fibroblast growth factor 1 (FGF1)
Intracellular function
Protein–protein interaction
p53
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:
02 Oct 2023
02 Oct 2023
Historique:
received:
21
05
2023
accepted:
12
09
2023
revised:
28
08
2023
medline:
4
10
2023
pubmed:
3
10
2023
entrez:
2
10
2023
Statut:
epublish
Résumé
Fibroblast growth factor 1 (FGF1) acts by activating specific tyrosine kinase receptors on the cell surface. In addition to this classical mode of action, FGF1 also exhibits intracellular activity. Recently, we found that FGF1 translocated into the cell interior exhibits anti-apoptotic activity independent of receptor activation and downstream signaling. Here, we show that expression of FGF1 increases the survival of cells treated with various apoptosis inducers, but only when wild-type p53 is present. The p53-negative cells were not protected by either ectopically expressed or translocated FGF1. We also confirmed the requirement of p53 for the anti-apoptotic intracellular activity of FGF1 by silencing p53, resulting in loss of the protective effect of FGF1. In contrast, in p53-negative cells, intracellular FGF1 regained its anti-apoptotic properties after transfection with wild-type p53. We also found that FGF1 directly interacts with p53 in cells and that the binding region is located in the DBD domain of p53. We therefore postulate that intracellular FGF1 protects cells from apoptosis by directly interacting with p53.
Identifiants
pubmed: 37783936
doi: 10.1007/s00018-023-04964-9
pii: 10.1007/s00018-023-04964-9
pmc: PMC10545594
doi:
Substances chimiques
Fibroblast Growth Factor 1
104781-85-3
Tumor Suppressor Protein p53
0
Receptor Protein-Tyrosine Kinases
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
311Subventions
Organisme : Narodowe Centrum Nauki
ID : 2015/18/E/NZ3/00501
Organisme : Narodowe Centrum Nauki
ID : 2018/31/N/NZ3/02257
Organisme : Narodowe Centrum Nauki
ID : 2020/02/Y/NZ3/00028
Informations de copyright
© 2023. The Author(s).
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