FGF13A interacts with NPM1 and UBF and inhibits the invasion of bladder cancer cells.
Bladder cancer
Fibroblast growth factor 13A
NPM1
Nucleolus location
UBF
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
20 10 2023
20 10 2023
Historique:
received:
30
06
2023
revised:
06
08
2023
accepted:
17
08
2023
medline:
18
9
2023
pubmed:
22
8
2023
entrez:
21
8
2023
Statut:
ppublish
Résumé
Bladder cancer (BC) invasion is a critical factor that impacts the prognosis and quality of life of patients. However, the underlying mechanisms of BC invasion is far from clear. Fibroblast growth factor 13 (FGF13), a non-secretory FGF, has been found to be ectopically expressed in various tumors and implicated in tumor development, but its potential association to BC has not been investigated. Here, we reported that the expression of FGF13A, one nucleolar isoform of FGF13, was downregulated in BC patients and negatively associated with tumor invasion. Additionally, we demonstrated that overexpression of FGF13A could inhibit the migration and invasion of BC 5637 and T24 cells. We also confirmed the localization of FGF13A in the nucleolus and its interaction with nucleoproteins NPM1 and UBP. Subsequently, we identified that the N-terminal region of FGF13A was essential for its nucleolus location and interaction with NPM1. Furthermore, we found that FGF13A inhibited the generation of nascent ribosomal RNA and suppressed the migration and invasion of BC cells through its N-terminal region. Our research establishes, for the first time, a correlation between the expression of FGF13A and the onset and progression of BC. This provides novel insights into the role of FGF13A in the development of BC.
Identifiants
pubmed: 37603967
pii: S0006-291X(23)00986-5
doi: 10.1016/j.bbrc.2023.08.040
pii:
doi:
Substances chimiques
fibroblast growth factor 13
330E71H5Q4
NPM1 protein, human
0
Nuclear Proteins
0
Protein Isoforms
0
transcription factor UBF
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-10Informations de copyright
Copyright © 2023. Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.